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Chapter 25

Chapter 25


Department
Neuroscience
Course Code
NROC61H3
Professor
Le Boutillier
Chapter
25

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CHAPTER 25 – MOLECULAR MECHANISMS OF LEARNING AND MEMORY
Introduction
studies on invertebrate animals have shown that Hebb was right: memories can reside in synaptic
alterations
theoretical work studying the brains mechanism in regard to memories has shown that
activity-dependent synaptic plasticity in the adult brain have a lot in common with those
operating in development for wiring of the brain
basic molecular mechanisms that alter that alter synaptic effectiveness are similar to
memory formation mechanisms in invertebrates
Procedural Learning
procedural memories have characteristics that make them more ideal to study verses declarative
memories
not easily forgotten
formed along simple reflex pathways that link sensations to movement
typically broken down into two categories
nonassociative learning – describes the change in behavioral response that occurs over
time in response to a single type of stimulus
habituation – learning to ignore a stimulus that lacks meaning due to its repeated
presentation
sensitization – learning to intensify response to all stimuli, even those that
previously evoked little or no reaction
associative learning – associations are formed between events
classical conditioning – associating a stimulus (US) that evokes a measurable
response (UR) with a second stimulus (CS) that normally does not evoke this
response, but will evoke a response (CR) after being repeatedly paired with a US
timing requirements
US and CS presented simultaneously or if CS precedes US by a
short interval
instrumental conditioning – association of a response, a motor act, with a
meaningful stimulus (e.g. food reward)
timing is important
Simple Systems: Invertebrate Models of Learning
reasons why invertebrate animals offer important experimental advantages
small NS, large neurons, identifiable neurons, identifiable circuits, simple genetics
nonassociative learning in Aplysia (sea slug)
habituation of gill withdrawal reflex
sensory info from siphon – abdominal ganglion – motor neurons + interneurons
one motor neurons that receives direct input is L7 and this cell innervates
muscle that produces the withdrawal effect
where does habituation occur
at the sensory nerve endings of the skin, making them less sensitive to
water squirt
ruled out because these endings continue to fire AP despite
motor response decrease
at the muscle making it less sensitive to synaptic stimulation by motor
neuron
ruled out because electrical stimulation of L7 always evoked the
same amount of muscle contraction
at the synapse between the sensory and motor neuron
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seems to be the case because giving repetitive stimulation to
sensory neuron was sufficient to cause decrease in size of post-
synaptic EPSP
where is the synapse modified after habituation
less NT release by presynaptic axon
this seems to be the case; fewer quanta (packets of NT) is
released per AP after habituation
decrease postsynaptic response to NT
ruled out; sensitivity did not change
THEREFORE habituation of gill-withdrawal reflex is die to PRESYNAPTIC
modification
this is due to the entry of Ca2+ which become persistently less effective
following habituation
sensitization of gill-withdrawal reflex
to cause sensitization a brief electrical shock to the head was given which
resulted in exaggerated gill-withdrawal in response to siphon stimulation
modification of NT release in sensory nerve terminal causes sensitization
why does showing the head promote sensitization
L29 which is activated by head shock make synapse on the axon terminal
of SENSORY neurons
L29 releases serotonin which SENSITIZES axon terminal causing it to
let MORE Ca2+ in per AP
serotonin receptor on sensory axon terminal is a G-protein-
coupled metabotropic receptor that leads to production of
intracellular secondary messengers (cAMP)
cAMP activates protein kinase A which phosphorylates K+
channel causing it to close
closure leads to extension of presynaptic AP = more Ca2+ entry
= more quanta of NT released
associative learning in Aplysia
Aplysia could be classically conditioned
US = strong shock to tail
CS = gentle stimulation of siphon which normally would not cause much of a
response
both are paired causing exaggerated gill-withdrawal due to sensitization
and eventually CS alone would cause withdrawal
critical modification occurs at the synapse between the sensory and motor neuron
at CELLULAR level, CS is represented by arrival of AP in the sensory
axon terminal and US is represented by the release of serotonin by L29
at MOLECULAR level CS is represented by INFLUX of Ca2+ and US is
represented by G-coupled activation of adenylyl cyclase in the terminal
(see nonassociative learning)
in the presence of elevated [Ca2+] adenylyl cyclase releases
more cAMP which closes more K+ channels causing more NT
release
according to this
LEARNING occurs when presynaptic Ca2+ pulse coincides (or just
precedes) activation of adenylyl cyclase which stimulates production of a
lot of cAMP
MEMORY occurs when K+ channels are phosphorylated and NT release
is enhanced
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