Search for notes by fellow students, in your own course and all over the country.
Browse our notes for titles which look like what you need, you can preview any of the notes via a sample of the contents. After you're happy these are the notes you're after simply pop them into your shopping cart.
Title: Physiology of Memory
Description: This notes will help you understand the physiology of memory that you will need when you learn about neuroscience. I compiled the notes from Guyton and Hall texbook of physiology and other neuroscience books.
Description: This notes will help you understand the physiology of memory that you will need when you learn about neuroscience. I compiled the notes from Guyton and Hall texbook of physiology and other neuroscience books.
Document Preview
Extracts from the notes are below, to see the PDF you'll receive please use the links above
MEMORY PHYSIOLOGY!
!
Learning is acquisition of the information that makes this possible and memory is the retention and
storage of that information
...
The new or facilitated pathways are called
memory traces, once they are established, they can be selectively activated by the thinking mind to
reproduce the memories
...
!
Positive memory!
: Information that causes important consequences such as pain or pleasure,
!
!
!
the brain has automatic capability of enhancing and storing the memory !
!
!
!
traces
...
!
!
FORMS OF MEMORY!
Priming: facilitation of the recognition of words or objects!
!
Explicit memory and implicit memory involve:!
1
...
It is caused by continual neural activity resulting
from nerve signals that travel around and around a temporary memory trace (circuit of
reverberating neurone), another possible explanation: presynaptic inhibition which occurs in the
synapses that lie on terminal nerve fibrils immediately before these fibrils synapse with a
subsequent neuron, the neurotransmitter chemicals secreted causes inhibition lasting for
seconds up to several minutes
...
Intermediate long-term memories: which last for days to weeks but then fade away
...
It results from temporary chemical or physical change in either the synapse
presynaptic terminals or the synapse postsynaptic membrane, changes that can persist for a
few minutes up to several weeks
...
Long term memory: Which stores memories for years and sometimes for life
...
!
!
Structural changes that occur in the synapses during the development of long term memory:!
!
Increase in vesicle release sites for secretion of transmitter substance!
Increase in number of transmitter vesicles released!
Increase in number of presynaptic terminals!
Changes in structures of dendritic spines that permit transmission of stronger signals!
!
4
...
!
!
Working memory keeps incoming information available for a short time while deciding what to
!
do with it
...
!
! It consists of what has been called a central executive located in the prefrontal cortex, and two
!
“rehearsal systems:” a verbal system for retaining verbal memories and a parallel visuospatial
!
system for retaining visual and spatial aspects of objects
...
it
evokes less and less electrical response as it is repeated
...
!
When the sensory terminal is stimulated repeatedly but without stimulation of the facilitator
terminal, signal transmission at first is great but it becomes less and less intense with repeated
stimulation until transmission almost ceases
...
LTD is the opposite of LTP, it is characterised by a
decrease in synaptic strength, it is produced by slower stimulation of presynaptic neurone and
associated with smaller rise in intracellular Ca2+ than in LTP
...
It is the prolonged occurrence of augmented
postsynaptic responses after a stimulus that has become habituated is paired once or several
times with a noxious stimulus
...
!
Facilitation mechanism:!
1
...
!
2
...
It causes the formation of cAMP
...
cAMP activates protein kinases that causes phosphorylation of a protein that itself is part of
potassium channels in the sensory synaptic terminal membrane
...
!
4
...
!
5
...
It causes greatly increased transmitter
!
release by synapse
...
The long-term potentiation (LTP) also involves protein
synthesis and growth of the presynaptic and postsynaptic neurone and their connections
...
-> AMPA activation relieves the Mg2+ block in the NMDA receptor channel
-> Ca2+ and Na+ enters the neuron -> Increase in cytoplasmic Ca2+ activates calmodulin kinase,
protein kinase C, and tyrosine kinase -> LTP!
!
Calmodulin kinase II phosphorylates AMPA receptors -> Increase their conductance -> AMPA
receptors move into the synaptic cell membrane from cytoplasmic storage sites
...
!
!
NEUROGENESIS!
During the first few weeks, months, and perhaps even year or so of life, many parts of the brain
produce a great excess of neurons and the neurons send out numerous axon branches to make
connections with other neurons
...
Thus, the number of neuronal connections is
determined by specific nerve growth factors released retrogradely from the stimulated cells
...
” That is, the short-term memory if activated repeatedly will
initiate chemical, physical, and anatomical changes in the synapses that are responsible for the
long-term type of memory
...
!
Studies have shown that rehearsal of the same information again and again in the mind
accelerates and potentiates the degree of transfer of short-term memory into long-term memory
and therefore accelerates and enhances consolidation
...
Output from the hippocampus leaves via the subiculum and the entorhinal cortex and
strengthens circuits in many neocortical areas, forming stable remote memories that can be
triggered by various cues
...
!
!
Anterograde amnesia: Difficulty making new memories and absorbing new information
...
With it, you cannot convert
new sensory information into long-term memories
...
Drinking too much alcohol blocks the neural pathways
in the brain from forming new memories while intoxicated
...
!
!
Retrograde amnesia: When retrograde amnesia occurs, the degree of amnesia for recent events is
likely to be much greater than for events of the distant past
...
!
Damage in the thalamic!
: Retrograde without anterograde amnesia!
Lesions in the hippocampal! : Retrograde + anterograde amnesia!
A possible explanation of this is that the thalamus may play a role in helping the person “search”
the memory storehouses and thus “read out” the memories
...
!
Dissociative amnesia: People involved in a serious car crash or victims of violent crimes
sometimes cannot remember the incident
...
!
Intense, prolonged stress can lead to dissociative amnesia because it activates our adrenal glands,
which release cortisol and other hormones into the bloodstream
...
Extended exposure to cortisol can negatively affect the hippocampus [source: Canadian Institute of
Neuroscience, Mental Health and Addiction]
...
!
!
Neurological amnesia is caused by damage to the areas of our brain that create memories: the
cortex -- particularly in the temporal lobe -- and the hippocampus
...
When this kind of amnesia occurs, it's like cutting a telephone line
...
!
If there is no pathway for the information to travel across, the brain cannot form new memories or
retrieve some old ones
...
A brief loss of oxygen flow to the brain, for instance, may leave someone
unable to remember only a few hours
Title: Physiology of Memory
Description: This notes will help you understand the physiology of memory that you will need when you learn about neuroscience. I compiled the notes from Guyton and Hall texbook of physiology and other neuroscience books.
Description: This notes will help you understand the physiology of memory that you will need when you learn about neuroscience. I compiled the notes from Guyton and Hall texbook of physiology and other neuroscience books.