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Transmission of electric impulses through bio membranes
Living organisms react with their environment (both internal and external) through conveying signals
in the form of electrical impulses through neurons (the cells which form the nervous system in many
organisms)
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Nerve cells convey the electrical impulses rapidly
(around 100m/s) which means that the information conveyed by the nervous system is much more
rapid than the information conveyed by the endocrine system
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Integration: this is the interpretation
step where the incoming sensory
input is processed and sent from the
CNS through the PNS (through motor
neurons) to the target cells
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The
dendrites are processes extending from the perikaryon, their function is to percept the chemical
signals and convey them as electrical impulses across the neuron along the length of the axon
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Membrane and action potentials:
The membrane potential is achieved due to the difference in the electrical charges between the
inside and the outside of the cell
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The cell normally
has higher chemical concentrations of
potassium ions within its cytoplasm,
K+ leak channels are present on the
membrane that allow for potassium
to flow along its chemical gradient
leaving negatively charged anions
(like proteins) in the cell and
increasing the concentration of
positively charged potassium on the
outside
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Equilibrium is
reached when the electrical gradient is equal to the chemical gradient which stops the flow of
potassium, this state is called the equilibrium potential (the equilibrium potential for potassium is
normally -96mV, for sodium is +60mV and for chloride is -70mV)
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Depolarization of the membrane can lead to signal propagation
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These ion channels allow for the flow of ions in and out of the cell
deviating the potential of the membrane away from its resting phase
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Inhibitory
ligand channels allow the exit of K+ which decreases membrane potential making it more negative
(hyperpolarizing)
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When
the membrane potential hits the threshold voltage (-55mV), voltage-gated sodium channels at the
axon hillock (implantation cone) open up increasing the influx of sodium into the cell and rapidly
increasing the membrane potential, the cell is now entering the depolarization phase where the
membrane potential changes from -70mV till it reaches maximum action potential of around
+30mV (action potential peak)
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However, when resting potential is
reestablished, the voltage gated potassium channels
stay open for a little longer which further decreases
membrane potential below its resting -70mV
potential, this is the hyperpolarization phase
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If the
sodium/potassium pumps were not present, the
electrochemical gradient won’t exist and the
membrane potential would be 0mV
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The refractory period
is the period where neurons cannot process an action potential because the ion pumps are occupied
in propagating an electric impulse
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The absolute
refractory period starts from the
potential threshold (-55mV) and ends
when the neuron gets back to resting
potential before hyperpolarization
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At this period, it is
possible to generate an action potential
but it requires a strong stimulus
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But during hyperpolarization (assuming
that the hyperpolarization peak is -90mV), the difference between the threshold and
hyperpolarization peak potentials is 20mV
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Note: no matter how strong the stimulus is, an action potential can never be generated during the
absolute refractory period
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This is what’s known as graded potential
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The neighboring segment get depolarized in return and
also achieves action potential
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The speed of nerve impulse propagation:
Myelination of the axons can increase the speed of nerve impulse propagation by up to 20x
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In vertebrates, many axons are
myelinated (the myelination is not continuous, it is discontinuous where two myelin sheaths are
separated by a node of Ranvier)
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The functioning of sodium and potassium
pumps only occurs at the nodes of Ranvier
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Synapses can be classified into
electrical and chemical synapses
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At the level of the synapse, it is observed that the two neurons are adhered to each other
by gap junctions, these gap junctions allow the passive flow of ionic current from one neuron to
another (direct propagation of potential)
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Chemical synapses contain three elements:
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Presynaptic element
Post synaptic element
Synaptic cleft

The presynaptic element contains voltagegated calcium channels, when the action
potential reaches the terminal bulb these
calcium channels open and allow for Ca++ ions
to enter the bulb
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The
neurotransmitters then diffuse through the synaptic cleft and bind to specific ligand-gated channels
on the postsynaptic element
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In order for an action potential to be
generated, the EPSP must be sufficient enough to pass through the threshold barrier in the
implantation cone (axon hillock; point where axon emerges from the soma) of the post synaptic
element
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One PSP (post synaptic potential) is sometimes
not enough to trigger an action potential hence the formation of multiple synapses
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There are two types of PSP summations, temporal and spatial summations
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Spatial summation is the
cumulative EPSPs generated by several pre synaptic elements
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Synapses are not permanent elements, they undergo changes as the organism evolves where old
synapses disappear as they are no longer used while new connections are constantly being
established, Damage done to synapses can lead to neurological disorders like Alzheimer’s
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Acetylcholine is synthesized from choline and acetyl-CoA by the action of choline acetyltransferase
(ChAT)
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Sometimes Ach is synthesized in the perikaryon where its packages in vesicles (quanta) and
sent to the nerve endings through OAF
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Ach binds to cholinergic receptors found at the post synaptic element and generate an
action potential (when the summation of Ach generated PSP is sufficient to pass the threshold)
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Note: the loading of Ach into their vesicles is done by a transporter called vesicular acetylcholine
transporter (VAchT)

Noradrenergic synapses contain the neurotransmitter noradrenaline (NorAd)
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Vesicular monoamine transporters (VMT) load NorAd into vesicles in the nerve endings, when
calcium influx is generated, exocytosis of NorAd is achieved, at the level of the synaptic cleft, NorAd
binds to its noradrenergic receptors in the post synaptic element, excess NorAd undergoes reuptake
into in the presynaptic element through Norepinephrine Transporter (NET) found on the presynaptic
element or it can be catabolized by monoamine oxidase (MAO) [intracellularly inside a
mitochondrion] or through catechol-O-methyltransferase (COMT) [at the synaptic cleft]
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Usually, neurotransmitters are terminated from the synaptic cleft through diffusion, degradation or
reuptake
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They activate a signaling pathway that involves the
function of a kinase (through production of cAMP) that phosphorylates proteins that closes K+
channels which leads to longer times of stimulation and longer recuperation (to return to resting
potential) times

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