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Psych 202
Unit 1
 Introduction
 Biopsychology – definition, goals
o Relates behavior to bodily processes
o Main goal: to understand the brain structures and functions that respond to experiences and generate
behavior
o Phrenology: localization of function
o Systematic description of behavior
o The evolution of brain and behavior
 Evaluating similarities among species and by looking at differences due to adaptions to different
environments
o Life-span development of the brain and behavior
 Ontogeny: process by which an individual changes in the course of its lifetime
o The biological mechanisms of behavior
 How
 5 research perspectives
o Neuroplasticity: the ability of the nervous system to change in response to an environment
o Social neuroscience: an emerging discipline that uses the tools of neuroscience to discover how biological
and social factors continually interact and affect each other as behavior unfolds
 Testosterone
o Evolutionary psychology: how natural selection has shaped behavior in humans and other animals
 How to test
o Epigenetics: focusing on factors that have a lasting effect on patterns of gene expression (the turning off
or on of specific genes) without changing the structure of the genes themselves
o Neuro-economics: the study of brain mechanisms at work during economic decision making (playing
games, managing resources, etc
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It seeks to identify which human psychological traits are evolved adaptations –
that is, the functional products of natural selection or sexual selection
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o MRI: uses magnetic energy to generate images that reveal some structural details in the living brain
 Higher resolution and fewer damaging effects
 Subtler changes
o Function MRI: detects changes in blood flow and therefore identities regions of the brain that are
particularly active during a given task
 Images of brain activity
o Pet: combines tomography with injections of radioactive substances used by the brain
 Faster and able to track quick changes
o TMS: applies strong magnetic fields to stimulate cortical neurons, in order to identity discrete areas of the
brain that are particularly active during specific behaviors
o MEG: measure the tiny magnetic fields produced by active neurons, in order to identity regions of the
brain that are particularity active during a given task
Division of the central nervous system:
o Forebrain
 Telencephalon
 Diencephalon
o Midbrain
 Mesencephalon
o Hindbrain
 Metencephalon
 Mylencephalon

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Forebrain: contains the telencephalon (cerebral hemispheres) and diencephalon
o Telencephalon: cortex, basal ganglia, limbic system
 Cerebral cortex: thick sheet of brain tissue, mostly neurons and their fibers
 Surrounds the cerebral hemisphere
 Divided into four lobes
o Gyrus: ridges of tissue
o Sulcus: crevices
o Fissure: large grooves
 Frontal lobe
o Prefrontal cortex
 Higher cognitive functions
o Motor association cortex
 Anterior to the PMC (in front of)
 Plans movement
o Primary motor cortex
 Controls contralateral motor output
 Somatopic organization
 Controls opposite side
 Parietal lobe
o Primary somatosensory cortex
 Receives contralateral sensory input
 Somatopic organization
o Somatosensory association cortex
 Located posterior
 Somatosensory perception and memories
 Temporal lobe
o Primary auditory cortex
 Receives auditory input
o Auditory association cortex
 Analyzes auditory information
 Auditory perception and memory storage
 Occipital lobe
o Primary visual cortex
 Receives input from contralateral visual field
o Visual association cortex
 Surrounds PVC and extends into the central temporal lobe
 Analyzes visual information
 Visual perception and memory storage
 Limbic system: loosely define, widespread network of structures that are involving in emotion
and learning
 Amygdala: emotional regulation and perception of odor
 Hippocampus: learning and memory (as well as fornix and mammillary bodies)
 Fornix: fiber tract that extends to the mammillary body, also important for learning for
memory
 Nucleus accumbens: reinforcement
 Cingulate cortex: direction of attention
 Olfactory bulb: sense of smell
 Basal ganglia: a group of forebrain nuclei, including the caudate nucleus, the putamen, and the
globus pallidus, that plays a critical role in the control of movement
 Caudate: largely responsible or voluntary movement
 Putamen: regulate movements and influence various types of learning
 Globus pallidus: constant subtle regulations
 Striatum: subcortical part of the forebrain
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Mostly receives and
processes information
o Dorsal horn: found at all spinal cord levels and is comprised of sensory nuclei that receive and process
incoming somatosensory information
o Ventral horn: motor neurons that innervate skeletal muscle
White matter: myelin, mostly transmits information
Each spinal nerve consists of:
o Motor efferent (output)
o Sensory afferent (input)
o Splits into a dorsal and ventral root
Dorsal root
o Carries info into the sensory axon

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Dorsal root ganglion: where the cell body is
Axon enters the spinal cord and either:
 Continues up the brain
 Synapses in the dorsal horn
Ventral root
o Carries the motor axon
o Cell body in the ventral horn of the spinal cord no ventral root ganglia
o Axon carries motor information out to the periphery
Divisions of the peripheral nervous system:
o Consist of nerves that extend throughout the body
o Motor nerves: transmit information from the spinal cord and brain to the muscles and glands
o Sensory nerves: convey information from the body the CNS
o Cranial nerves: connect directly to the brain
 12 pairs
 Sensory and motor functions of the face, head, neck, and throat
o Spinal nerves: connected at regular intervals to the spinal cord
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o Somatic NS
 Carrying motor and sensory information to and from the CNS
 Sensory input
 Motor control
 Afferent (relaying sensation to the CNS) and efferent (stimulation muscle contraction )
 Spinal nerves, cranial nerves, association nerves
o Autonomic: nerves that connect the internal organs
 Sympathetic nervous system
 Fight or flight
 Utilization of energy resources
 Parasympathetic
 Rest and digest
 Conservation of energy resources
Lateralization of function
o Different areas of the brain are specialized for different things
o Labels of being right or left brained not supported—both hemispheres contribute to different kinds of
processes
o Left / right handed
 A person's preferred hand is not a clear indication of the location of brain function
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8% of left-handed
people have right-hemisphere dominance for language function
Neural tube: an embryonic structure with subdivisions that correspond to the future forebrain, midbrain, and
hindbrain
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Most common type
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Sensory systems only

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Unipolar: single extension that branches in two directions after leaving the cell body
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From body into spinal cord, sensory
Innervate
o To provide neural input to
o Most neurons have an axon hillock from which the axon projects, this hillock gathers and integrates
information from the synapses and converts them into a code of electrical impulses that race down the
axon toward targets
Glial cells in the adult brain – (astrocytes, oligodendrocytes/Schwann cells, microglia) & functions of each
o Glial cells outnumber neurons
o Oligodendrocytes (in the brain and spinal cord) and Schwann cells: wrap around axons to provide myelin,
a fatty insulating substance (improves the speed at which nerve impulses are conducted)
o Nodes of Ranvier: gap between successive segments of myelin sheath where the axon membrane is
exposed
o Astrocytes: weave around and between neurons with tentacle-like extensions, controlling local blood flow
to increase the amount of blood reaching more-active brain regions, modulate neural activity and
formation of synapses, forming outer membranes that swaddle the brain
 Nourishment and support
 Problem when they swell in response to injury
o Microglial: tiny and mobile, contain and cleanup site of injury
 Glial scars
Problems associated with glial cells (MS, glial scars, swelling)
o MS: interferes with myelin
o They continue to divide into adulthood, can give rise to deadly brain tumors, and can create glial scars
that create a wall, problem especially in the spinal cord
o Respond to brain injury by changing size, leading to swelling (edema)
Blood brain barrier – structure and function
o The mechanisms that make the movement of substances from blood vessels into brain cells more difficult
than exchanges in other body organs, thus affording the brain greater protection from exposure to some
substances found in the blood
o Capillaries in the brain are highly resistant to the passage of large molecules across their walls and
neighboring regions
o Composed of tightly packed cells and astrocytes
o Semipermeable: drugs, hormones
Withdrawal reflex
o Sensory neuron detects the pain stimulus
o Message is sent to the terminal buttons on the spinal cord
o Message is passed to an interneuron inside the spinal cord
o Interneuron passes the message to a motor neuron
o Motor neuron sends a message to contract the muscle
Membrane potential
o The difference in electrical charge between the inside and outside of a cell
Polarization: a difference in electric charge between the inside and outside of a cell
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These concentration gradients provide the potential energy to
drive the formation of the membrane potential
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Electrostatic forces

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The propensity of charged molecules or ions to move, via diffusion, toward areas with the opposite charge
Diffusion: force that causes molecules of a substance to spread from regions of high concentration to
regions of low concentration
o Go towards equal concentration
o So, cations like potassium are attracted to the negatively charged interior of the cell, and anions are
repelled
o Positive exterior attracts anions, repels cations
Sodium/potassium pump
o Energetically expensive mechanism that pushes sodium ions out of a cell, and potassium ions in
o Pumps three sodium ions out for every two potassium ions pumped in
o Buildup of K ions inside the cell, but K ions can leave the interior, moving down their concentration
gradient and causing a net buildup of negative charges inside the cell, exerting electrostatic pressure to
pull positively charged K ions back inside, leading to equilibrium potential: any further movement of K
into the cell is matched by movement out
Selective permeability
o The property of a membrane that allows some substances to pass through, but not others
o Some ion channels stay open all the times, but the cell membrane of a neuron contains many such
channels that selectively allow only potassium ions to cross the membrane
Voltage-gated ion channels
o Ion channels are pores in the cell membrane that permits the passage of certain ions through the
membrane when the channels are open
o A Na selective channel that opens or closes in response to changes in the voltage of the local membrane
potential; it mediates the action potential
o When the cell membrane becomes depolarized the threshold levels, the gates channel changes, opening
the gate to allow Na ions through
o Voltage gated K channels then allow K ions to rush out quickly, restoring the resting potential
o Regenerated along the length of the axon, so normally goes in only one direction, because leaves in its
wake refractory membrane
o Charge: electrical: within
Ligand-gated ion channels
o Sodium and potassium
o Chemical: between
o Open in response to a ligand binding to them
Depolarization
o A decrease in membrane potential (the interior becomes less negative) –moving the membrane potential
closer to zero
Hyperpolarization
o An increase in membrane potential (the interior of the neuron becomes more negative) –making the
potential even farther from zero
EPSPs (depolarization)
o A depolarizing potential in the postsynaptic neuron that is caused by excitatory presynaptic potentials
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this depolarization is known as EPSP, because it pushes the
postsynaptic cell a little closer to the threshold for an action potential
o Increase in the charge inside of the cell reduces resting potential (less polarized, closer to zero)
IPSPs (hyperpolarization)
o A hyperpolarizing potential in the postsynaptic neuron that is caused by inhibitory connections
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If this summation reaches threshold, an action potential is triggered
o ESPS and ISPS do tend to cancel each other out
o But potentials spread passively and dissipate as they cross the cell membrane, the resulting sum is also
affected by distance
o Temporal summation: the summation of postsynaptic potentials that reach the axon hillock at different
times
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At its peak, the action potential approaches
the equilibrium potential for NA: about plus 40
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The resulting flow of ions creates a local
EPSP or IPSP in the postsynaptic neuron
o The IPSP and ESPS in the postsynaptic cell spread toward the axon hillock (if the sum of it all
depolarizes the hillock enough to reach threshold, an action potential will arise)
o Synaptic transmission is rapidly stopped, so the message is brief and accurately reflects the activity of the
presynaptic cell
o Synaptic transmitter may also activate presynaptic receptors, resulting in a decrease in transmitter release
o Class
 Action potential arrives at the terminal button

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 Voltage gated CA channels open, CA enters the axon terminal
 Synaptic vesicles binds o the inside of the presynaptic membranes
 Vesicles rupture, release NT into the synaptic cleft
 NT binds to the receptor
 Prompting specific ion channels to open
 NA: goes inside, more positive
 K: goes outside, more negative
 Cl: ligand gated, goes inside, more negative
 Post synaptic potentials are produced by the flow of ions in and out of the cell
 Each NT produces a specific postsynaptic potential
o Excitatory NT bind to receptors that open Na ion channels
 Produce a depolarizing excitatory postsynaptic potential
o Inhibitory NTs bind to receptors that open K and / or Cl ion channels
 Produce an IPSP
 Changes in the charge of the postsynaptic membrane
 Neural integration is the summation of all post synaptic potentials
 Spatial summation and temporal summation
 Determines the absolute effect of the axon hillock
 If the cell is depolarized to the threshold of excitation  an action potential fires
 If the cell is hyperpolarized  nothing happens
 Removal of NT from the synapse terminates PSPs
 Reputake
o Transporter molecules draw NT back into the cell
 Enzymatic deactivation
o Enzyme in the synapse breaks down NT molecules
Ionotropic receptor
o Ligand attaches to binding sites
 Ion channels open very quickly, but close quickly
Metabotropic receptor
o Ligand attaches to binding site
 Activates a G-protein
 Activates an enzyme
 Produces a second messenger
 Opens the ion channel—open longer, but stays closed longer
Excitatory & inhibitory neurotransmitters
o A transmitter can function is either or at different synapses
o As an excitatory synapse, opens channels for Na and K
o At inhibitory, allowed chloride ions to enter, hyperpolarizing
Reuptake
o Two ways to bring transmitter effects to a prompt halt
o Degradation: transmitter molecules rapidly broken down and thus inactivated by special enzymes
o Reuptake: absorbed back into the axon terminal that released the
o Transporters bring them back inside
Enzymatic deactivation (ACh & AChE)
o Acetylcholinesterase breaks down acetylcholine
Autoreceptors
o Found on the presynaptic membrane
 Bind NTs released by the same cell
 Monitor synaptic activity
 Regulate the amount of NT released
Types of synapses – structure & function
o Axo-dendritic: a synapse at which a presynaptic axon terminal synapses onto a dendrite of the
postsynaptic neuron, either via a dendritic spine or directly onto the dendrite itself

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Axo-somatic: axon to cell body
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Components of the ERP tend to be reliable because the background noise of the cortex has been
averaged out
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Doesn’t involve the entire brain, so can have a wide variety of symptoms

Unit 2
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Know the definitions and functions of the following terms, concepts and systems
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Psychopharmacology
Pharmacokinetics: movement of a drug into the body and out of
Routes of administration (general description of each, as well as specific route of administration for drugs
discussed in class and the text)
o Bioavailable
 Smoking or intravenous injection ramp up the amount of drug that is free to act on the target
tissue, and not in use elsewhere or in the process of being eliminated
o Biotransformation
 Swallowing: concentration of a drug builds up slowly over longer periods of time
 How the drug is metabolized: vid kidneys, liver, lungs, or other routes
 Enzymes convert a drug into a metabolite that is itself active, perhaps in ways that are different
from original
o Blood-brain barrier
 Can block useful drugs
Factors affecting drug effectiveness
o Binding affinity : a particular drug will generally being strongly to one kind of receptor, more weakly to
other types, and not at all to many others
 High doses: enough molecules are available to bind to both low and high affinity receptors
o Efficacy: once it is bound, the drug has a certain propensity to activate the receptor
 Agonists: high efficacy
 Antagonists: low or no efficacy
o Combination of affinity and efficacy that determine effect
o Dose-response curve: greater doses tend to produce greater effects
 Effective dose 50: dose at which drug shows half its maximum effect
 Therapeutic index: separation between effective doses of a drug and the toxic doses
 Bigger separation: safer

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Exogenous: substances from external sources
Endogenous: a substance from an internal source (NT)
Agonists: facilitate synaptic transmission
o Drugs: not always ligands at post synaptic receptors, but always affecting transmission in one of two
ways
Antagonists: inhibit synaptic transmission
Sites of action
o Drug effects on production of neurotransmitter (NT)
 Precursors are synthesized into NT at the soma or axon terminal
 Agonists: act as precursors
 Increase NT production
 Antagonist: inactivate the enzymes required for NT synthesis
 Decrease NT production
o Drug effects on storage of NT
 NTs are packed into vesicles by transporter molecules on the desired membrane
 Antagonists: inactivate these transporter molecules to prevent storage of the NTs
 Vesicles are empty: no NT will be released into the synapse
o Drug effects on release of NT
 CA ions are required for a vesicle to fuse with the presynaptic membrane and rupture (exocytosis)
 Agonists: act directly on the vesicle, causing exocytosis
 More NT is released
 Antagonists: block exocytosis
 NT is not released
o Drug effects on receptors & autoreceptors
 NTs: bind to binding sites on post-synaptic receptors to open ligand-gated channels
 Competitive agonists: bind to the NT binding sites
 Activate the receptor, opening ion channels
 Results in a PSP (Na for ESPS, Cl or K for ISPS)
 Competitive antagonists: block the NTs binding sites
 Prevent NTs from binding with the receptors
 Prevents opening of ion channels
 Some receptors contain multiple sites, where other endogenous ligands may bind
 Noncompetitive agonists: bind to different binding sites on the receptor
o Activate the receptor, opening ion channels
o Results in a PSP
 Noncompetitive antagonists: bind to different binding sites on the receptor
o Inactivate the receptor
o Prevents opening of ion channels
o Drug effects on termination of synaptic transmission
 Agonists: inactivate the transporter molecule for reputake or deactivate the enzymes that break
down NT
 Both mechanisms keep NT in the synapse longer
 Antagonist???
Amines: all below
o NT based on modifications of a single amino acid nucleus
o Acetylcholine, serotonin, dopamine
o Monamines and the subclasses
 Norepinephrine, epinephrine
Acetylcholine (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Cholinergic: Ach containing neurons are found in nuclei within the basal forebrain
o Project to sites such as the cerebral cortex, amygdala, and hippocampus
o Widespread loss is associated with Alzheimer’s disease
o Made in cell bodies located in:

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Motor neurons: ventral horn
 Released at neuromuscular junctions
 Controls muscle contractions
 Pons
 Project to cortex and thalamus
 Controls cortical arousal and REM sleep
 Basal forebrain
 Projects to the hippocampus, amygdala, cortex
 Facilitates learning and memory
o Acts on nicotinic and muscarinic receptors
o Drug effects
 Agonists: stimulate the CNS, cause muscle contractions
 Nicotine
o Competitive agonist at nicotine ACH receptors
o Increase CNS function
 Muscarine
o Competitive agonist at muscarinic ACH receptors
o Causes convulsions
 Neostigmine
o Reactivates ACHE, blocking breakdown of ACH
o Pesticide
o Used to treated myasthenia gravis: lets ACH stay longer
 Antagonists: block muscle contractions
 Botulinum toxin (Botox)
o Prevents the release of ACH
o Causes paralysis
 Curare
o Competitive antagonist at Nicotinic ACH receptors
o Causes paralysis
Monoamines
o Major class of compounds, each derived from a single amino acid
o Two subclasses:
 Catecholamines (derived from tyrosine)
 Dopamine
 Norepinephrine
 Epinephrine (hormone  adrenaline)
 Indolamines (derived from tryptophan)
 Serotonin
 Melatonin (hormone)
Dopamine (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Three major systems:
 Mesostriatal pathway
 Cell bodies in the substantia nigra of the midbrain
 Axons project to the striatum
 Motor control  loss can lead to Parkinson’s disease
 Mesolimbic system
 Cell bodies in the ventral tegmental area
 Axons project to the nucleus accumbens, amygdala, and hippocampus
 Reinforcing effects of rewards
 Mesocortical system
 Cell bodies in the ventral tegmental area
 Axons project to the pre-frontal cortex
 Attention, formation of short-term memories, planning and problem solving

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 Acts on DA receptors (D1- D5)
Drug effects
 Agonists: increase attention, energy, reward, and motor control
 L-Dopa
o Da precursor
o Improves motor function in Parkinson’s disease
 Cocaine, Amphetamine, Adderall
o Stimulate between release and prevent reuptake (transporter molecule moves
backwards)
o Causes euphoria, heightened arousal, energy, focus, deceased appetite, psychotic
symptoms
 Ritalin
o Prevents reuptake: stalls transporter
o Increases attention
 Antagonists: decrease psychotic symptoms
 Typical antipsychotic drugs (Chlorpromazine)
o Competitive antagonist at DA D2 receptors
 Atypical antipsychotics (Clozapine)
o Competitive antagonists at DA and other NT receptors
Norepinephrine (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Made in cell bodies located in:
 Locus Coeruleus (pons)
 Project to cortex, limbic system, thalamus, cerebellum, spinal cord
 Responsible for mood, arousal, and vigilance
 Lateral tegmental system (midbrain)
 Project to the hypothalamus
 Involved in endocrine system
o Act on alpha and beta adrenergic receptor
o Effects
 Agonists: increase arousal and mood
 Methamphetamines
o Stimulates NE and DA release and prevents reuptake
o Causes euphoria, increased arousal, energy and preservation, loss of appetite,
irritability and agitation, long term damage to many body systems
 Bupropion (Wellbutrin / Zyban)
o Prevents reuptake of NE and DA
o Competitive antagonist at nicotinic ACH receptors
o Anti-depressant, smoking cessation
 Antagonists: decrease sympathetic nervous system activity
 Propranolol
o Competitive antagonist at B-adrengic receptors
o Decease symptoms of stress (PTSD)
Serotonin or 5 - HT (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Made in cell bodies in the raphe nuclei on the midbrain
 Axons project widely throughout the brain
 Involved in regulation of mood, control of appetite, sleep, dreaming, arousal, and pain regulation
o Acts on 19 plus types of 5 – HT receptors throughout the brain
o Drug effects
 Agonists: increase positive mood, decrease anxiety, distort perception
 LSD, DAAT, Psilocybin
o Competitive agonists at 5 – HT receptors
o Cause hallucinations
 MDMA (Molly)
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Reverse the 5-HT, DA, and NE transporter molecules
Causes euphoria, decreased anxiety, feelings of well-being, empathy, intimacy,
cognitive impairment
 Selective 5 –HT reuptake inhibitors (most common for depression)
o Prevent 5-HT reuptake
o Improve mood, decrease anxiety when used long term
 Antagonists: decease psychotic symptoms
 Atypical antipsychotics (Clozapine, Quetiapine)
o Competitive antagonists at 5 –HT, DA, and other NT receptors
Amino acid neurotransmitters
o Amino acid produced be cell metabolism act as NT
o Two major amino acid NT: Glutamate and GABA
Glutamate (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Major excitatory NT found through the brain
 Increase depolarization at post-synaptic neurons
o Acts on receptors
 NMDA, AMPA, Kainite, and Metabotropic
o Directly affects other axons
 Lowers the threshold of excitation
 Less depolarization is needed to produce an action potential
o Agonists: increase CNS activity
 Eglumedgad
 Competitive agonist at metabotropic GLU receptors
 Decrease anxiety and psychotic symptoms
o Antagonists: decrease CNS activity
 Alcohol
 Competitive antagonist at NMDA receptors
 Depresses CNS activity
 PCP and Ketamine
 Noncompetitive antagonists at NMDA receptors
 Cause dissociation, interrupt thought, memory formation, and produce psychotic
symptoms
GABA (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Major inhibitory NT found throughout the brain
 Increase hyperpolarization at post-synaptic neurons
o Acts on receptors
 GABAa and GABAb
o Directly effects other axons
 Raises the threshold of excitation
 More depolarization is needed to produce an action potential
o Agonists: depresses CNS activity
 Alcohol, benzodiazepines, barbiturates, GHB
 Competitive and noncompetitive GABA receptor agonists (Alcohol agonist at GABAa
and GABAb)
 Produces sleep, anxiety, relief, muscle relaxation, seizure alleviation
o Antagonists: increase CNS activity
 Bicuculine
 Competitive antagonist at GABAa receptor
 Produce seizures, used to study epilepsy
Neuropeptides
o A neurotransmitter consisting of a short chain of amino acids (see below)
Endogenous opioids (characteristics, receptors, drug effects at various sites of action)
o Enkephalins, dynorphin, endorphins

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Made in cell bodies in the hypothalamus and brain stem
 Axons project to the
 Periaqueductal gray area
o Produce analgesia (pain relief)
 Limbic system
o Mediate reinforcement and pleasure
 Hypothalamus
o Influence endocrine control of eating, sleeping, sex
o Act on mu, delta, and kappa opiate receptors
o Agonists: powerful analgesics
 Opium, morphine, heroine, oxycodone, and other narcotics
 Competitive agonists at the opiate receptors
 Produce analgesia, hypothermia, sedation, and euphoria
 Rapidly lead to tolerance and intense withdrawal symptoms
o Antagonists: block the effects the opiates
 Naloxone and naltrexone
 Competitive antagonists at opiate receptors
 Used to treat opiate overdose and addiction
Endocannabinoids (characteristics, origination and transport, receptors, drug effects at various sites of action)
o Lipid-based neuromodulators, not traditional neurotransmitters
o Produce on demand in the post synaptic membrane
o Transmit messages between cells via retrograde transport
o Work throughout the CNS and PNS to motivate neural activity
 Involved in cognition, mood, pain sensation, appetite, movement
o Act on CB1 and CB2 cannabinoid receptors found in the presynaptic membrane
o Agonists: modulate numerous systems
 Marijuana (THC)
 Competitive agonist at the CB receptors
 Psychoactive- interferes with concentration, memory, and perception, may produce mild
euphoria and / or hallucinations
 Increases analgesia, sedation, and appetite, decreases anxiety, prevents excitotoxicity
during stroke
o Antagonists: limit modulatory actions of the endocannabinoids
 Rimonabant
 Competitive antagonist t the CB1 receptor
 Used to treat obesity
Addiction: dependence on a particular substance of activity
Perspectives on drug abuse
o Moral model: addiction is the result of weakness and lack of self-control
o Disease model: medical treatment
o Physical dependence model: people keep taking drugs in order to avoid unpleasant withdrawal symptoms
o Positive reward model: people get started with drug abuse, and become addicted, because the abused drug
provides powerful reinforcement
Diagnostic criteria for dependence and substance abuse
o Dependence: a cluster of cognitive, behavioral, and psychological symptoms indicating that the individual
continues use of the substance despite significant substance-related problems
 Must meet three of seven criteria:
 Patterns of consumption
 Craving
 Expenditure of time and energy in serving the addiction
 Impact on others aspects of the person’s life
o Substance abuse: minimum criteria have not been met but patterns of abuse have persisted at least a
month, diagnose is substance abuse

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Tolerance: decreased behavioral effectiveness, more drug is needed
o Metabolic tolerance: body getting used to the drug being present
 Body becomes more effective at eliminating the drug before it can have an effect
o Functional tolerance
 Down-regulation of receptors: taking away receptors, repeated used of agonist
 Up-regulation of receptors: more receptors, repeated used of antagonist
 Withdrawal: symptoms occur in response to absence of the drug
o Specific effects for each drug (basically, the opposite)
 Sensitization: increased behavioral effectiveness, less drug is needed
o Results from long-term structural changes in the brain
 Growth of dendrites
 Synaptogenesis: increased conductivity in nucleus accumbens or reward centers
o Brain responds more strongly to the drug and associated drug cues
o Both tolerance and sensitization
 Physical dependence
o When the body requires the drug in order to function normally
o Reduction of physical withdrawal symptoms become a reason for continued use of the drug
 Psychological dependence
o When the mind requires the drug in order to gain the psychological effects that it produces
o Cravings: psychological fixation on obtaining the drug
 Associated with long term changes in the brain
 Persists after long periods of abstinence
 Psychological dependence is much more enduring than physical
o Not all drugs physical, but all addiction has a psychological component physical can be stopped, but
physiological cannot
 Reinforcement
o Drugs of abuse are reinforcing
 Act-directly or indirectly- to promote dopamine release in the mesolimbic system
 Between acting at the nucleus accumbens produces positive, reinforcing feelings
 Results in the desire to take the drug again
 Act quickly, reinforcing the action of taking them
o Removal of withdrawal symptoms is also psychologically reinforcing
 Genetics and addiction
o Common genetic factors: predispose a person to addiction
...

o Specific genetic factors
 Genetically determined traits influence personal response to a drug: how you react
 Attention deficit hyperactivity disorder
 Drugs additional – clue section with TA
1
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Agonist: increase the NT effect
i
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Antagonist decrease the NT effect
c
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L Dopa is the only precursor
e
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Will still bind, just nothing in them
g
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Curare: competitive antagonist
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Non-competitive: bind to a different spot, NT can still bind
k
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Ritalin: prevents reuptake, NOT stimulate DA release
m
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Agonist in both NE and DA symptoms would likely to:
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Inocbye rimosa
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Neuromodulators: modulation mean change, neuro means
q
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dark is created by the drain in response to many factors
Primary visual pathway
o Each eye receives stimulation from both halves of the visual field, inverted on the retina
o Receptor cells in the left half of each retina respond to stimuli in the right visual field and vice versa
o Retinal ganglion cell axons combine in the optic nerve to carry this input to the brain
o At the optic chiasm, axons from the medial halves of the retina cross to the contralateral optic tract, while
axons from the lateral halves continue to the ipsilateral optic tract (retinal ganglion cells known after they
pass the optic chiasm)
o Axons carrying information from the left visual field proceed to the right literal geniculate nucleus where
they synapse (right visual field  left LGN)
o Neurons in the lateral geniculate nucleus project to the primary visual cortex
 `LGN is the visual part of the thalamus
 The PVS is also called striate cortex or V1
Retino-hypothalamic pathway
o Suprachiasmtic nucleus: synchronizes circadian rhythms
Retino-tectal pathway
o Coordinates eye movement and muscles of the iris and lens
Striate cortex (V1)
o The first cortical stop for incoming visual information
o Striate cortex contains a map of the contralateral visual field
 Disproportionate representation of the fovea
o Each retinal ganglion cell responds to its own receptive field
 Portion of the visual field
o LGN neurons receive information from multiple retinal ganglion cells
o Striate neurons receive information from multiple LGN neurons
 Integration allows for visual perception of orientation, movement, depth, and color
o Orientation-sensitive neurons only respond to objects in a particular spatial placement
 Simple cells: detect orientation
 Complex cells: detect orientation and movement
Receptive field (concentric nature)
o The stimulus region and features that affect the activity of a cell in a sensory system
o Neurons in the retina and LGN have concentric receptive fields
 Roughly circular central area and a ring around it
 Photoreceptors in the central area and those in the ring surrounding it tend to have opposite
effects on the next cells in the cirui
Binocular vision
o Provides the most acute depth-perception
o Stereopsis: the process by which both eyes coordinate to perceive depth
o Many neurons in the visual cortex respond to visual stimulation from both eyes
o Retinal disparity: slightly different images falls on each retina
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Binocular cells respond strongly to retinal disparity: slightly different angles hitting left and right
eye
 Disparity indicates distance between the object and observer, allows perception of depth
Cytochrome oxidase blobs
o Information from color-sensitive ganglion cells is transmitted to specialized cells grouped together as
cytochrome oxidase blobs in the striate cortex
 CO blobs contain wavelength-sensitive neurons
 Central in color vision processing in some species
V1 modules
o Striate cortex is organized into modules
o Each module contains neurons that analyze information from a single region of the visual field
 Each module receives input from both eyes
 Neurons in each module share the same ocular dominance (amount of input from each eye)
 Eyes receiving synaptic input
 Neurons with the module are highly connected and mostly binocular
 Each module is centered around a CO blob, surrounded by neurons sensitive to orientation,
movement, and depth
Extrastriate cortex
o Visual association cortex
o Combines information from individual modules in V1
 Perception
o Two streams of visual information project from V1 to extrastriate cortex:
 Dorsal: recognized where an object is located
 Ventral visual stream: recognizes what the object is
Color perception
o In the dorsal stream:
 Movement: perception mediated by neurons in area V-5 (medial temporal area)
o Perception in the ventral stream:
 Form: perception is mediated by neurons in area V2, V4, and the inferior temporal lobe
 Color: perception is mediate by extrastriate neurons in area V 4
Mirror neurons
o Important in the understanding of other individual’s actions
o Empathy
Visual agnosias
o Damage to the visual associated cortex can result in a visual agnosia: the inability to perceive or identify a
stimulus, despite normal visual sensation
 Achromatopsia: damage to the extrastriate cortex in the medial occipital lobe may result in loss of
color vision
 Akinetopsia: damage tom V5 can result in the inability to perceive movement
 Apperceptive visual agnosia: inability to perceive and identity common objects by sight
 Prosopagnosia: inability to identify a familiar face
Scotoma: if we know the site of injury in the visual pathway, we can predict the location of such a perceptual gap
(region of blindness within the visual fields)

Unit 3

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Hormones and reproductive behavior
Endocrine gland
o A gland that secretes products into the bloodstream to act on distant targets
Allomone: made in your body, effect a different species

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Pheromones – effects in animals and humans
o Chemicals released outside the body to affect other individuals of the same species
o Dogs and wolves urinating
Hormones
o Amine hormone: single amino acid
o Peptide hormone (protein): peptide strand of amino acids
o Both activate receptors on the surface of a cell membrane
o Activate second messengers that lead to changes in cell function
Steroid hormone: synthesized from cholesterol, lipid-soluble
o Binds to receptors inside the cell membrane because they can easily pass through cell membranes
 Transported into the nucleus where it targets the DNA to influence protein production
HPA axis
o Hypothalamic – pituitary – adrenal axis
o Paraventricular nucleus of the hypothalamus, which contains neuroendocrine neurons that synthesize and
secrete vasopressin and corticotrophin-releasing hormone
Hypothalamus, hormones produced
o Neurons in the hypothalamus produce hormones that travel to the pituitary
o Growth-hormone releasing hormone
Anterior pituitary, hormones produced
o Releasing hormones from the hypothalamus enter the hypothalamic –pituitary portal system which
delivers that hormone to the anterior pituitary (entirely glandular—hormones)
o Hypothalamic releasing hormones act on anterior pituitary cells to prompt secretion of tropic hormones
into the blood stream—blood-brain barrier
o Hypothalamus secretes releasing hormones, anterior pituitary secretes tropic hormones  target glands
o Hypothalamus
 Gonadotropin releasing hormones (GnRH)
o Anterior pituitary
 Gonadotropic hormones
 Follicle stimulating hormones (FSH)
o Stimulates growth of the gracifian follicle (contains eggs) and developing ovum
in the ovary
o Stimulates sperm production in the testes
 Luteinizing hormones
o Stimulates production of estrogen in the ovary
 Stimulates the follicles of the ovary to rupture, release eggs, and form
into structure called corpora lutea that secrete progesterone
o Stimulates production of testosterone in the testes
o Hypothalamus
 Thyrotrophin releasing hormone
o Anterior pituitary
 Prolactin
o Stimulates progesterone production in the ovary
o Stimulates milk production in mammary glands
Posterior pituitary, hormones produced
o Does not itself produce hormones
 Axons from the supraoptic nucleus and paraventricular nucleus of the hypothalamus (HPA axis)
terminate on capillaries found in the posterior pituitary—releasing hypothalamic hormones
directly into the blood stream
 Axons from the hypothalamus terminate on capillaries found in the posterior pituitary: releasing
hypothalamic hormones directly into the blood stream
o Vasopressin
 Antidiuretic hormones
 Prompts fluid retention in the kidneys
 Vasoconstrictions

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 Increases blood pressure
 Facilitates bonding
o Oxytocin
 Stimulates contractions of the uterus during childbirth and breastfeeding
 Stimulates milk letdown during breastfeeding
 Released during orgasm
 Facilitates bonding
 Impairs memory
Ovaries & testes as glands, hormones produced (puberty)
o Puberty begins when the hypothalamus begins to secrete gonadotropic releasing hormone
o Ovulatory cycle beings when FSH stimulates ovarian follicles to grow and secrete estrogens  induce the
hypothalamus and pituitary to release LH  triggers ovulation
 Corpora lutea secretes progesterone to maintain the uterus for pregnancy
o GnRH stimulates the anterior pituitary to release gonadotropic hormones (LH and FSH)
 Gonadotropic hormones stimulate the gonads to release sex hormones
 Ovaries: estradiol, progesterone, and some androgen
o Also produce eggs
 Testes: androgen and a little estradiol
o Also produce sperm
 Development of secondary sex characteristics is directed by gonadal hormones
 Estradiol: typical female
 Androgen: typical male, body hair
o Testes
o Adrenal glands: everybody, same amount of androgen and estrogen
Reproductive behavior
o Sexual attraction
 Males and females are attracted to one another based off of appearance, behaviors, and sent
o Appetitive behavior
 Behaviors that display and maintain sexual interest
 proceptive
o Copulation
 Intromission
o Postcopulatory behaviors
 Refractory period: sexual arousal not possible
 Copulatory lock: some species, gets stuck
Sexual differentiation and dimorphism
o Sexual differentiation: the process by which individuals develops either male like or female like bodies
o Sexual dimorphism: the condition in which males and females of the same specie show pronounced sex
differences in appearance
 Androgen masculinizes the brain region, and absence of androgen leads to a female-typical brain
anatomy
 Brain regions controlling sexually distinct behaviors are organized by prenatal hormone exposure
 Androgen exposure: masculinization of neural circuitry
 If not exposed to androgens, female-typical circuitry develops
 Distinct brain regions
 Sexually dimorphic nucleus of the preoptic area
o Females: smaller: ovulatory cycles
o Males: larger: copulatory behaviors
 Spinal nucleus of the bulbocavernsus
o Females (smaller): female sexual behavior or no effect
o Males (larger): appetitive sexual behaviors
 Medial amygdala
o Females (smaller): proceptive and maternal behaviors

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Males (larger): appetitive sexual behaviors

Development and definition of primary sex organs (gonads, internal sex organs, external sex organs)
o Primary sexual development occurs in five stages
 At each stage, bio potential structures are masculinized or feminized into sexually dimorphic
organs
 Genes and hormones direct
o Stages
 Chromosomes
 23rd pair: sex chromosomes
 Gonads
 Produce hormones and gametes
 Internal reproductive organs (connect gonads to the outside)
 External genitalia
 Brain
o Chromosomes
 Chromosome complement is present at conception
 XX (females )or XY (males) (or other)
o Gonads
 Are undifferentiated through the 6th week of prenatal development
 SRY gene on the Y chromosome  development of testes
 No SRY gene and XX chromosomes
 SRY gene: testes
 No SRY gene: ovaries
 Gonads begin to produce sex-specific hormones immediately
 Prenatal development: sex hormones exert organizational effects
 Puberty: sex hormones exert activational effects
o Internal sex hormones
 All embryos have precursors for both male and female internal sex organs
 Early fetus has a genital tubercle that can become either a clitoris or penis, as well as two sets of
ducts: the wolffian and mullerian
 Testicular hormones stimulate development of male internal sex organs
 Androgen (testosterone) has a masculinizing effect
o Wolffian ducts  epididymis, vas deferens, and seminal vesicles
 Antimullerian hormone has a defeminizing effect
o Mullerian ducts recede
 If no hormones are secreted, the Mullerian ducts will develop in to the female internal
reproductive organs

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 Fimbriae, fallopian tubes, uterus, and upper 2/3 of the vagina
External sex organs
 The presence of androgen results in the development of male external genitalia (DHT, promoted
by 5 alpha reductase)
 Penis and scrotum
 The absence of androgen results in the development of female extern genitalia
 Labia, clitoris, and lower 1/3 of the vagina
Intersex conditions
o Turner syndrome (female)
 Only one x chromosome is present at conception
 Female internal reproductive
 Female external
 Shorter
 No ovaries: no spontaneous puberty
o Persistent mullerian duct syndrome (male)
 Failure to produce anti-mullerian hormone in an XY individual
 Androgen is present
 Mullerian ducts develop
 Not often recognized
o Androgen insensitivity syndrome (female)
 Lack of androgen receptors in an XY individual
 Androgen and antimullarian hormone are present
 No masculinization effects
 No internal reproductive organs
 Female external
 Typical female puberty
o Congenital adrenal hyperplasia (female)
 Adrenal glands of genetic females secrete abnormally high amounts of androgen, starting during
gestation
 Partially or entirely masculinized: ambiguous
o 5 alpha reductase deficiency (female  male) (guervedoces –testes at 12 years)
 Lack of 5 alpha reductase prevents conversion of testosterone into (more potent)
dihydrotestosterone (DHT)
 Prevents masculinization of external genitalia during prenatal development
 Penis / scrotum in puberty
Organizational/Activational effects
o Activational: a temporary change in behavior resulting from the administration of a hormones to an adult
animal
o Organizational: a permanent alteration of the nervous system, and thus permanent change in behavior,
resulting from the action of a steroid hormones on an animal early in its development
Sensitive period: the period during development in which an organism can be permanently altered by a particular
experience or treatment
o Specific
Castration and effects
o Castration: removal of the gonads, usually the testes
o Aristotle and chickens
 Castrating means failure to develop normal reproductive behaviors
o Arnold Berthold
 Returning one testis back into the body cavity allowed them to develop normal male sexual
behaviors
 Because testes make and secrete testosterone
Cloacal exstrophy
o Genetic boys are born with functional testes but without penises
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o Raised as girls, but many wanted to become boys later in life
Coolidge effect
o Propensity of an animal that has appeared sexually satisfied with a present partner to resume sexual
activity when provided with a new partner
Major findings of Alfred Kinsey and Masters & Johnson on human sexual behavior
o 1940’s: Kinsey began to ask friends and colleagues about their sexual history
o Nearly all men masturbated, that college-educated people were more likely to engage in oral sex than one,
many people had at one time or another engaged in homosexual behaviors, and that 10 percent preferred
o Masters and Johnson
 Variety of reproductive behaviors that distinguish human sexuality
 Orgasm
 Increasing excitement, plateau, orgasm, and resolution
 Women: three typical patterns, men only have one
 Men: absolute refractory phase following orgasm
 Women: can have multiple in rapid succession
 Women: governed more by emotional factors
Major histocompatibility complex
o May be related to mate choice in some human populations
o Olfaction: MCH phenotype appears strongly involved in the strength and pleasantness of perceived odor
of compounds from sweat
o Smelling t shirts
Sexual orientation (hormonal & genetic influence; evidence for this)
o Prenatal hormone exposure appears to influence sexual attraction
o Evidence from individuals with disorder affecting prenatal hormone exposure
 Congenital adrenal hyperplasia
 Masculinizing effect in the brain and external genitalia
 Correlated with a higher than average lesbian attraction
 Androgen insensitivity syndrome
 No androgen receptors in the brain –prevents masculinization in humans
 Individuals look and feel female, tend to be very feminine and almost always oriented
towards males
o Orientation may be genetically influenced
 Concordance: 52 % concordance rate of homosexual orientation in identical male twins, 48 % in
female identical twins
 May be exerted through prenatal hormone exposure
 Caveat: research has only looked at this in gays and lesbians
 No data on concordance rates for heterosexual orientation
 Several markers have been correlated with gay and lesbian attractions, but most of these strongly
overlap with opposite-sex attraction
 No studies have looked specifically for markers correlated with opposite sex attraction
Aromatization hypothesis
o Testosterone and estradiol molecules are very closely related in structure—testosterone is the precursor
for the manufacturing of estradiol in the ovary
o Aromatization: the enzyme aromatase converts testosterone to estradiol (and other androgens to other
estrogens)
o Testicular androgens enter the brain and are converted there in estrogens
o Estrogens are prevented from entering into the brain
o Lack of aromatase: plays a role in unusual sexual differentiation of the spotted hyena
Parental behavior (hormonal and neural control)
o All mammals must take care of newborns in order to ensure survival
o Parental behaviors are species-specific
 Rats and many other lower mammals engage in:
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 Licking
 Crouching over pups to nurse
 Retrieving pups
 Dams do this automatically, other rats may do it following prolonged exposure to the pups
o Males (hormonal control of reproductive behavior)
 Male copulatory behavior depends on the presence of testosterone (in all mammalian species)
 In lower mammals, the female must be receptive
 Males parental behavior varies greatly among species
 Oxytocin and vasopressin contribute to pair-bonding and paternal behaviors
o Females (hormonal control of reproductive behavior)
 Lower mammals: female sexual behavior depends on the presence of estradiol
 Peak estradiol secretion (at ovulation) results in:
o Attractiveness: changes that affect the male
o Proceptivity: eagerness to copulate
 Ear wagging and hopping
o Receptivity: willing/ able to copulate
 Lordosis reflex occurs in the presence of a male rate
 Curvature of the spine, etc
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Projects to:
 Periaqueductal gray area
 Behavior response (emotional)
 Lateral hypothalamus
 Autonomic (sympathetic) response
 Bed nucleus of the stria terminalus (BNST)
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Aggressive behaviors (characteristics, neural & hormonal control, role of serotonin, evidence for these)
o Behavioral response involving threatening gestures or an attack on another animal
o Aggressive behaviors are species specific
 Related to both reproduction and self-defense
 Behavioral expression is controlled by neural circuits in the PAG region
 Dorsal PAG: controls defensive behaviors
 Ventral PAG: controls predatory behaviors
o Amygdala activation is associated with human anger and aggression
 Normally mediated or suppressed by the prefrontal cortex
o Prefrontal cortex
 PC regulates emotional expression
 Recognizes the emotional significance of complex social situations
 Inhibits impulses and regulates behavioral response
o Orbitofrontal cortex
 Critical to emotional regulation
 Translates judgment and conclusions about the environment into behavioral and
physiological responses
o Medial prefrontal cortex
 Critical to emotional reasoning
 Consideration of ethical situations
 Damage to the prefrontal cortex results in bad emotional regulation
 Poor impulse control, impaired social responses, aggression, and violence
 Antisocial personality disorder is correlated with a reduction in grey matter of the
prefrontal cortex
o Role of serotonin
 Prefrontal serotonin activity inhibits aggression, impulsivity, and risk taking behaviors
 Low 5HT activity increases these behaviors
o Juvenile monkeys with low 5HT show increased risk taking behavior and
aggressive attacks on dominant monkeys
 Impulsive behavior  death
o Mice lacking 5HT receptors exhibit increased aggression against other mice
o In humans, low levels of 5HT are correlated with assault, arson, murder, child
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Measured in patients with personality disorders and a history of
impulsive aggression
Serotonin agonists decrease irritability, aggressiveness, and impulsivity on
psychological measures

Stress hormones
o Prenatal androgen exposure organizes neural circuits controlling aggression
 At puberty, testosterone activates these circuits, increased aggressive behaviors
o Medial preoptic area
 Projects to the PAG
 Critical to reproductive and defensive behaviors
 Stimulation by testosterone produces aggression
 High concentration of androgen receptors
 Injection of testosterone increases internal aggression
o Androgen
 Androgen levels are associated with impulsive behaviors and aggression in humans
 Puberty: spike in impulsive behaviors
 High testosterone associated with hostility
 Female convicts: high testosterone associated with unprovoked violence, low testosterone
associated with defensive crimes
 Anabolic steroids: exogenous androgen associated with increased aggression
 Higher testosterone associated with dominance-related behaviors and wining
 Losing decreases testosterone levels
General adaptation syndrome
o Stress is a physiological and psychological response to a situation, not an emotion
o General adaptive syndrome: a close connection between stress and disease
 Alarm reaction (immediate response)
 Flight or fight
 Adrenaline, noradrenaline
 Cortisol: preparing the body for action
o Adaption stage
 Brings the body back to normal
o Exhaustion stage
 Prolonged or frequent repeated stress
 Susceptibility to illness
Stress and immune function
o Brain, endocrine system and immune system interact
o Brain stimulates cortisol and adrenaline release in response to a stressor
o Cortisol inhibits immune function
o Immune system is monitored and regulated by the brain
Influences on stress response
o Individuals vary in response to stress
 Genetic differences
 Perception of stress
 Stress immunization
 Small, early stressors, followed by maternal attention, makes rats more resilient to stress
in adulthood
 Maternal neglect or deprivation results in epigenetic alterations that makes rate and
humans hyper responsive and less resilient to stress in adulthood

Learning and memory
 Synaptic plasticity
o Learning: set of processes by which experience creates enduring changes to neural circuits, changing
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o Changes in synaptic structure and biochemistry
Long-term potentiation – definition, characteristics
o Potentiation: increased / strengthened effect
o Synaptic connections are strengthened by synaptic activity paired with depolarization in the postsynaptic
neuron
o Depends on the influx of calcium into the post synaptic receptor
o The CA channel on the NMDA receptor is blocked by a magnesium ion
o LTP is initiated if:
 The post synaptic membrane is depolarized
 Result of activity at AMPA receptors
 AND glutamate is bound to post-synaptic NMDA receptors
o Mg ion is released from NMDA receptor
 Calcium enters the post-synaptic membrane
o Ca acts as a second messenger in the post-synaptic membrane
 Activate protein kinases which direct
 Addition of AMDA receptors on the post synaptic membrane
 Addition of synapses between he pre and post synaptic neurons
 Increased glutamate release from the pre-synaptic membrane
o Retrograde transmitter
 These changes increase the effect of synaptic communication
 Increased likelihood of generating an action potential
o Synaptic strengthening is limited to those synapses where calcium entered the post-synaptic cell
o Once long-term potentiation has bene induced
 Synaptic transmission is more likely to cause an action potential in the post-synaptic neuron
 Lasts from several minutes to years
 Can be induced throughout the brain
Associative LTP – Hebb’s rule
o Neurons that fire together, wire together
o Simultaneous firing at a weak synapse and a strong synapse on the same post-synaptic neuron 
strengthens the weak synapse by association
 Depolarization by the strong synapse releases magnesium ions when glutamate is bound to
NMDA receptors at the weak synapse
o This is how associations are learned
NMDA receptor involvement in LTP (glutamate binding + dendritic spike = calcium influx)
Strengthening synapses – increased receptors, synaptogenesis, increased NT release – mechanisms of each
(Understand how these 3 changes relate to improved synaptic strength!)
Classifications of memory
o Declarative memory: explicit and readily available to conscious recollection
 Episodic: memories of events
 Semantic: memories of facts
 Spatial: memories of the location of objects
o Non-declarative memories: implicit, unconscious knowledge
 Priming: previous exposure to a stimulus
 Motor (skill): learned behavioral sequences
 Stimulus-response (associative): learned responses to specific stimuli
Perceptual learning – definition, characteristics, neural mechanisms/areas involved
Classical conditioning - definition, characteristics, steps of induction, neural mechanisms/areas involved, how this
demonstrates synaptic strengthening!
o Learning a specific behavioral response in the presence of a given stimulus
 Response to an association between 2 stimuli
 Simple, automatic responses
 Tone (neutral stimulus) + Foot shock (unconditioned stimulus) = freezing (unconditioned
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 Becomes tone (conditioned stimulus) = freezing (conditioned response)
Neural mechanisms
 LTP is exhibited in the amygdala following fear conditioned
 Lateral amygdala received weak input on the CS (tone) and strong input on the VS (foot shock)
 Strong VS synapses depolarize neurons in the lateral amygdala
 Produce an action potential in projections to the central amygdala (CAN)
 CAN: generates emotional response (VR: freezing)
 Repeated depolarization by the strong VS synapses paired with receptors activation at weak CS
synapses
 Strengthens CS synapses
 Connection between neuron signaling the tone and neuron signaling the behavioral response is
strengthened
 Firing at the tone synapses will now independently produce an action potential resulting
in freezing behavior
 PTSD  one trial
Motor learning - definition, characteristics, neural mechanisms/areas involved, how these change with
practice
o Motor cortex
o Areas can become larger with practice
Operant conditioning - definition, characteristics, role of reinforcement
o Learning to make a response in order to gain reinforcement or avoid punishment
 Formation of associations between discriminative stimulus, behavioral output, and resulting
consequences
 Discriminative stimulus signals opportunity
 Behavior occurs
 Reinforcing or punishing stimulus follows the behavior
o Animals learns to make the correct behavior in that context, in order to gain
reinforcement or avoid punishment
o Neural reinforcement mechanisms strengthen synapses between neurons that detect discriminative stimuli
and neurons that produce a behavioral response
o Nucleus accumbens receives
 Signals about the discriminative stimulus and behavior, contextual cues, from forebrain regions
 Weakly depolarizing
 Signals about reward from ventral tegmental area (medial forebrain bundle)
 Strongly depolarizing
 Simultaneous activation creates an association between contextual cues, behavior, and reward
 When activated, cells in the nucleus accumbens communicated with the striatum to initiate
behavior
 Drug addiction
Reinforcement – examples of reinforcement, neural circuitry & neurotransmitters involved, role in
strengthening synapses
Relational learning - definition, characteristics, types of learning, neural mechanisms/areas involved
o Complex learning involving associations between multiple stimuli, contexts, behaviors and outcomes
 Most learning involves relational learning
o Requires learning of individual stimuli and how
o each stimulus is related to the others
o Examples
 Episodic learning: establishing memories of experiences
 Spatial learning: forming memories of where objects are located
Spatial memory - definition, characteristics, role of hippocampus, how it is studied (examples)
o Memory of the location of objects and places in space
o Relies on the right hippocampal formation
 Damage to this are produces profound deficits in spatial memory
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Increased activity in this region while recalling spatial locations and navigating through an
environment
Hippocampal place cells
o Hippocampus is not necessary for most simple stimulus response learning, it is critical for relational
learning
o Studied in the Morris water maze – measure of spatial learning
 Animal model of relational learning
o Animals and humans with hippocampal lesions
 Can learn stimulus response tasks
 Cannot learn spatial relationships and cannot navigate according to contextual cues
Anterograde amnesia – definition, characteristics, development, brain regions, circuits and receptors involved
o Loss of relational learning ability
o New declarative memories are not formed
o Stimulus- response, perceptual, and motor learning abilities remain intact
o Most previously formed memories remain intact, though some retrograde amnesia is often seen
o Results from bilateral damage to, or removal of, the medial temporal area
 Contain the hippocampus—critical to memory formation
 Unilateral damage may produce minor memory deficits
o Famously studied in HM
 Both medial temporal lobes were removed to treat epilepsy
 Results in pervasive anterograde amnesia, accompanied by some retrograde amnesia
Retrograde amnesia
o Loss of previously formed declarative memories
Short-term memory
o Immediate and limited memory for recently perceived stimulus
 Holds 5 to 7 items for a few moments
 Indefinitely with rehearsal
Long-term memory
o Stable and unlimited memory for all learning
o Consolidation: shifts information from STM to LTM
 Hippocampus
Hippocampus – role in memory
o Not the location of long term memory storage
 HM long term memory was intact
o Not the location of short term memory storage
 Able to answer questions and hold info in his mind as long as he rehearsed it
o Involved in consolidation of long term memories
 Unable to form declarative memories

Final Review
Final Exam Study Guide
In addition to the list below, be sure to review your reading from the textbook
...
At its peak, the action potential approaches
the equilibrium potential for NA: about plus 40
...
The resulting flow of ions creates a local
EPSP or IPSP in the postsynaptic neuron
o The IPSP and ESPS in the postsynaptic cell spread toward the axon hillock (if the sum of it all
depolarizes the hillock enough to reach threshold, an action potential will arise)
o Synaptic transmission is rapidly stopped, so the message is brief and accurately reflects the activity of the
presynaptic cell
o Synaptic transmitter may also activate presynaptic receptors, resulting in a decrease in transmitter release
Summary
 Action potential arrives at the terminal button
 Voltage gated CA channels open, CA enters the axon terminal
 Synaptic vesicles binds to the inside of the presynaptic membranes
 Vesicles rupture, release NT into the synaptic cleft
 NT binds to the receptor
 Prompting specific ion channels to open
 NA: goes inside, more positive
 K: goes outside, more negative
 Cl: ligand gated, goes inside, more negative
 Post synaptic potentials are produced by the flow of ions in and out of the cell
 Each NT produces a specific postsynaptic potential
o Excitatory NT bind to receptors that open Na ion channels
 Produce a depolarizing excitatory postsynaptic potential
o Inhibitory NTs bind to receptors that open K and / or Cl ion channels
 Produce an IPSP

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 Changes in the charge of the postsynaptic membrane
Neural integration is the summation of all post synaptic potentials
 Spatial summation and temporal summation
 Determines the absolute effect of the axon hillock
 If the cell is depolarized to the threshold of excitation  an action potential fires
 If the cell is hyperpolarized  nothing happens
 Removal of NT from the synapse terminates PSPs
 Reputake
o Transporter molecules draw NT back into the cell
 Enzymatic deactivation
o Enzyme in the synapse breaks down NT molecules
Major divisions of the nervous system from telencephalon to myelencephalon
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Corpus callosum: main band of axons that connects the two cerebral hemispheres
o Coordinates sensory processing and motor output between hemispheres
Division of the central nervous system:
o Forebrain
 Telencephalon
 Diencephalon
o Midbrain
 Mesencephalon
o Hindbrain
 Metencephalon
 Mylencephalon
Forebrain: contains the telencephalon (cerebral hemispheres) and diencephalon
o Telencephalon: cortex, basal ganglia, limbic system
 Cerebral cortex: thick sheet of brain tissue, mostly neurons and their fibers
 Surrounds the cerebral hemisphere
 Divided into four lobes
o Gyrus: ridges of tissue
o Sulcus: crevices
o Fissure: large grooves
 Frontal lobe
o Prefrontal cortex
 Higher cognitive functions
o Motor association cortex
 Anterior to the PMC (in front of)
 Plans movement

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Primary motor cortex
 Controls contralateral motor output
 Somatopic organization
 Controls opposite side
 Parietal lobe
o Primary somatosensory cortex
 Receives contralateral sensory input
 Somatopic organization
o Somatosensory association cortex
 Located posterior
 Somatosensory perception and memories
 Temporal lobe
o Primary auditory cortex
 Receives auditory input
o Auditory association cortex
 Analyzes auditory information
 Auditory perception and memory storage
 Occipital lobe
o Primary visual cortex
 Receives input from contralateral visual field
o Visual association cortex
 Surrounds PVC and extends into the central temporal lobe
 Analyzes visual information
 Visual perception and memory storage
 Limbic system: loosely define, widespread network of structures that are involving in emotion
and learning
 Amygdala: emotional regulation and perception of odor
 Hippocampus: learning and memory (as well as fornix and mammillary bodies)
 Fornix: fiber tract that extends to the mammillary body, also important for learning for
memory
 Nucleus accumbens: reinforcement
 Cingulate cortex: direction of attention
 Olfactory bulb: sense of smell
 Basal ganglia: a group of forebrain nuclei, including the caudate nucleus, the putamen, and the
globus pallidus, that plays a critical role in the control of movement
 Caudate: largely responsible or voluntary movement
 Putamen: regulate movements and influence various types of learning
 Globus pallidus: constant subtle regulations
 Striatum: subcortical part of the forebrain
...
Most common type
...
Sensory systems only
 Unipolar: single extension that branches in two directions after leaving the cell body
...
From body into spinal cord, sensory
Stages of brain development
 Neurogenesis  cell migration  cell differentiation  synaptogenesis  apoptosis  synaptic
remodeling
Blood-brain: semipermeable
Dura matter: brain and spinal cord

Test 2
 Major roles of dopamine, norepinephrine, serotonin, acetylcholine, glutamate, GABA
o Agonists: facilitate synaptic transmission
 Drugs: not always ligands at post synaptic receptors, but always affecting transmission in one of
two ways
o Antagonists: inhibit synaptic transmission
 Acetylcholine
o Made in cell bodies located in:
 Motor neurons: ventral horn
 Released at neuromuscular junctions
 Controls muscle contractions
 Pons
 Project to cortex and thalamus
 Controls cortical arousal and REM sleep
 Basal forebrain
 Projects to the hippocampus, amygdala, cortex
 Facilitates learning and memory
o Acts on nicotinic and muscarinic receptors
o Drug effects
 Agonists: stimulate the CNS, cause muscle contractions
 Nicotine
o Competitive agonist at nicotine ACH receptors
o Increase CNS function
 Antagonists: block muscle contractions
 Botulinum toxin (Botox)
o Prevents the release of ACH
o Causes paralysis
 Curare
o Competitive antagonist at Nicotinic ACH receptors
o Causes paralysis
 Monoamines
o Major class of compounds, each derived from a single amino acid
o Two subclasses:
 Catecholamines (derived from tyrosine)

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 Dopamine
 Norepinephrine
 Epinephrine (hormone  adrenaline)
 Indolamines (derived from tryptophan)
 Serotonin
 Melatonin (hormone)
Dopamine (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Three major systems:
 Mesostriatal pathway
 Cell bodies in the substantia nigra of the midbrain
 Axons project to the striatum
 Motor control  loss can lead to Parkinson’s disease
 Mesolimbic system
 Cell bodies in the ventral tegmental area
 Axons project to the nucleus accumbens, amygdala, and hippocampus
 Reinforcing effects of rewards
 Mesocortical system
 Cell bodies in the ventral tegmental area
 Axons project to the pre-frontal cortex
 Attention, formation of short-term memories, planning and problem solving
 Acts on DA receptors (D1- D5)
o Drug effects
 Agonists: increase attention, energy, reward, and motor control
 L-Dopa
o Da precursor
o Improves motor function in Parkinson’s disease
 Cocaine, Amphetamine, Adderall
o Stimulate between release and prevent reuptake (transporter molecule moves
backwards)
o Causes euphoria, heightened arousal, energy, focus, deceased appetite, psychotic
symptoms
 Antagonists: decrease psychotic symptoms
 Typical antipsychotic drugs (Chlorpromazine)
o Competitive antagonist at DA D2 receptors
 Atypical antipsychotics (Clozapine)
o Competitive antagonists at DA and other NT receptors
Norepinephrine (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Made in cell bodies located in:
 Locus Coeruleus (pons)
 Project to cortex, limbic system, thalamus, cerebellum, spinal cord
 Responsible for mood, arousal, and vigilance
 Lateral tegmental system (midbrain)
 Project to the hypothalamus
 Involved in endocrine system
o Act on alpha and beta adrenergic receptor
o Effects
 Agonists: increase arousal and mood
 Methamphetamines
o Stimulates NE and DA release and prevents reuptake
o Causes euphoria, increased arousal, energy and preservation, loss of appetite,
irritability and agitation, long term damage to many body systems
 Antagonists: decrease sympathetic nervous system activity
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o Competitive antagonist at B-adrengic receptors
o Decease symptoms of stress (PTSD)
Serotonin or 5 - HT (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Made in cell bodies in the raphe nuclei on the midbrain
 Axons project widely throughout the brain
 Involved in regulation of mood, control of appetite, sleep, dreaming, arousal, and pain regulation
o Acts on 19 plus types of 5 – HT receptors throughout the brain
o Drug effects
 Agonists: increase positive mood, decrease anxiety, distort perception
 LSD, DAAT, Psilocybin
o Competitive agonists at 5 – HT receptors
o Cause hallucinations
 MDMA (Molly)
o Reverse the 5-HT, DA, and NE transporter molecules
o Causes euphoria, decreased anxiety, feelings of well-being, empathy, intimacy,
cognitive impairment
 Selective 5 –HT reuptake inhibitors (most common for depression)
o Prevent 5-HT reuptake
o Improve mood, decrease anxiety when used long term
 Antagonists: decease psychotic symptoms
 Atypical antipsychotics (Clozapine, Quetiapine)
o Competitive antagonists at 5 –HT, DA, and other NT receptors
Amino acid neurotransmitters
o Amino acid produced be cell metabolism act as NT
o Two major amino acid NT: Glutamate and GABA
Glutamate (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Major excitatory NT found through the brain
 Increase depolarization at post-synaptic neurons
o Acts on receptors
 NMDA, AMPA, Kainite, and Metabotropic
o Directly affects other axons
 Lowers the threshold of excitation
 Less depolarization is needed to produce an action potential
o Agonists: increase CNS activity
 Eglumedgad
 Competitive agonist at metabotropic GLU receptors
 Decrease anxiety and psychotic symptoms
o Antagonists: decrease CNS activity
 Alcohol
 Competitive antagonist at NMDA receptors
 Depresses CNS activity
 PCP and Ketamine
 Noncompetitive antagonists at NMDA receptors
 Cause dissociation, interrupt thought, memory formation, and produce psychotic
symptoms
GABA (characteristics, origination, systems, receptors, drug effects at various sites of action)
o Major inhibitory NT found throughout the brain
 Increase hyperpolarization at post-synaptic neurons
o Acts on receptors
 GABAa and GABAb
o Directly effects other axons
 Raises the threshold of excitation
 More depolarization is needed to produce an action potential

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Agonists: depresses CNS activity
 Alcohol, benzodiazepines, barbiturates, GHB
 Competitive and noncompetitive GABA receptor agonists (Alcohol agonist at GABAa
and GABAb)
 Produces sleep, anxiety, relief, muscle relaxation, seizure alleviation
o Antagonists: increase CNS activity
 Bicuculine
 Competitive antagonist at GABAa receptor
 Produce seizures, used to study epilepsy
Neuropeptides
o A neurotransmitter consisting of a short chain of amino acids (see below)
Endogenous opioids (characteristics, receptors, drug effects at various sites of action)
o Enkephalins, dynorphin, endorphins
o Made in cell bodies in the hypothalamus and brain stem
 Axons project to the
 Periaqueductal gray area
o Produce analgesia (pain relief)
 Limbic system
o Mediate reinforcement and pleasure
 Hypothalamus
o Influence endocrine control of eating, sleeping, sex
o Act on mu, delta, and kappa opiate receptors
o Agonists: powerful analgesics
 Opium, morphine, heroine, oxycodone, and other narcotics
 Competitive agonists at the opiate receptors
 Produce analgesia, hypothermia, sedation, and euphoria
 Rapidly lead to tolerance and intense withdrawal symptoms
o Antagonists: block the effects the opiates
 Naloxone and naltrexone
 Competitive antagonists at opiate receptors
 Used to treat opiate overdose and addiction
Endocannabinoids (characteristics, origination and transport, receptors, drug effects at various sites of action)
o Lipid-based neuromodulators, not traditional neurotransmitters
o Produce on demand in the post synaptic membrane
o Transmit messages between cells via retrograde transport
o Work throughout the CNS and PNS to motivate neural activity
 Involved in cognition, mood, pain sensation, appetite, movement
o Act on CB1 and CB2 cannabinoid receptors found in the presynaptic membrane
o Agonists: modulate numerous systems
 Marijuana (THC)
 Competitive agonist at the CB receptors
 Psychoactive- interferes with concentration, memory, and perception, may produce mild
euphoria and / or hallucinations
 Increases analgesia, sedation, and appetite, decreases anxiety, prevents excitotoxicity
during stroke
o Antagonists: limit modulatory actions of the endocannabinoids
 Rimonabant
 Competitive antagonist t the CB1 receptor
 Used to treat obesity
Sensitization and tolerance
Tolerance: decreased behavioral effectiveness, more drug is needed
o Metabolic tolerance: body getting used to the drug being present
 Body becomes more effective at eliminating the drug before it can have an effect

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Functional tolerance
 Down-regulation of receptors: taking away receptors, repeated used of agonist
 Up-regulation of receptors: more receptors, repeated used of antagonist
Withdrawal: symptoms occur in response to absence of the drug
o Specific effects for each drug (basically, the opposite)
Sensitization: increased behavioral effectiveness, less drug is needed
o Results from long-term structural changes in the brain
 Growth of dendrites
 Synaptogenesis: increased conductivity in nucleus accumbens or reward centers
o Brain responds more strongly to the drug and associated drug cues
o Both tolerance and sensitization
Addiction – physical and psychological
Physical dependence
o When the body requires the drug in order to function normally
o Reduction of physical withdrawal symptoms become a reason for continued use of the drug
Psychological dependence
o When the mind requires the drug in order to gain the psychological effects that it produces
o Cravings: psychological fixation on obtaining the drug
 Associated with long term changes in the brain
 Persists after long periods of abstinence
 Psychological dependence is much more enduring than physical
o Not all drugs physical, but all addiction has a psychological component physical can be stopped, but
physiological cannot
Ionotropic and metabotropic
o Metabotropic
 Second messenger
 Slower
 Both open when ligands attach to binding sites
Agonists: blocks autoreceptor
Noncompetitive antagonist: works on a different binding site to inactivate the receptor
Largest effect: a drug that causes NT release
L-Dopa works at production
Amino acid NT’s: work directly on the axonal membrane
Alcohol: inhibits neurons in the cortex and hippocampus
o Depressant which causes general CNS inhibition

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