Aplysia Flashcards
Why study aplysia
simple reflex behavior, only 20k large neurons
Siphon-gill withdrawl reflex
Tactile stimulus on mantle, gill and siphon withdraw to cavity
Nonassociative learning
Habituation - repeated stimuli gets smaller response
Dishabituation - restoration of habituated response after novel stimuli
Sensitization - strong stimulus results in exaggerated response to subsequent stimuli
Associative learning in withdrawal reflex
CS poke to siphon elicits response after conditioning
US shock elicits response
Poke must PRECEDE shock
CS precedes US, forward pairing
Aplysia neuroanatomy
all reflexes controlled by abdominal ganglion
How does sensitization affect synapse
Presynaptic faciliation
release more transmitter from sensory neuron
Shock the interneuron that synpases on sensory which goes to motor
Serotonin bath and cAMP inject to sensory also facilitates
How does sensitization work (list the neurochemical steps) 2 mechanisms
Serotonin binds on the sensory neuron
AP BROADENING - G protein activates adenyly cyclase makes ATP into cAMP
cAMP-dependent kinase PKA
PKA phosphorylates K channels, closing them
This makes the AP broaden and last longer, more CA entry and more NT released
NT RELEASE -
G protein activates phospholipase which activates PKC
PKC phosphorylates presynaptic proteins that add more vesicles to the releasable pool from the reserve pool = more NT release
Brain and behavior correlation
Amount of facilitation of the reflex in the synaptic potential is similar to the faciliation of behavior
Why should CS precede US
Activity dependent presynaptic facilitation
CS causes AP in the sensory neuron which allows for Calcium entry before shock stimulus
This binds calmodulin, increased adynly cyclase, more cAMP, more K channels phosp., more transmitter
adenylyl cyclase acts as COINCIDENCE detector, amplisifies sensory neuron response when CS and US occur together (cs preceding really)
Post synaptic factors
NMDA receptor on motor neuron needs glutamate to depol cell and open channel,
another coincidence mechanism (mg blocker with AMPA)
with NMDA antagonist, no facilitation
Both pre/post changes needed to allow learning
Ca entry in NMDA acts as retrograde signal back to act on adenylyl cyclase
Ca entry allows for NEW AMPA receptors in post
Long term faciliation changes (immed. early genes) CREB
Immediate early genes - act rapidly, proteins in nucleus act as transcription factors
Late response genes - activated for longer, proteins can leave nucleus
Catalytic subunit of PKA phosphyrlates CREB-1 which binds to cAMP activating IMMEDIATE EARLY GENES, cacase for late response long lasting structure changes
- Persistent activity of PKA, degrade regulatory subunit, doesn’t need cAMP anymore
- Growth of new synaptic connections
Learning mediated gene expression results in long term changes of connectivity
