7- synap phys 3 Flashcards
3 mechanisms for removing NT from synaptic clefts
1) diffusion (common in CNS and at NMJ) –> small molec diffuse into large ECF adjacent a
2) Reuptake (more impt in surrounding glia than NMJ) –> move into cell and then into vesicles
3) Destruction (more in NMJ than CNS for ACh)
- -> AChE –> choline and acetate –> reuptake
What is a coincidence detector
Example of one?
encode info by detecting spatially separated input signals
NMDA receptors bind glutamate, also have Mg2+ ion in pore
permeable to Ca2+
requires 2 simult signals
Mechanism of NMDA receptor activation
1) Glu from presynap bind NMDA and post-synap depol to force Mg out of pore
2) Ca2+ influx
How does Ca2+ ions in postsynap cell strengthen synapse?
insert additional AMPA receptors to allow neuron to respond more strongly to same amt of NT
from Ca2+ mediated fusion of postsynaptic vesicles containing AmPA in postsynap membrane
What is mechanism of presynaptic strengthening
1) NMDA recpetors activated and Ca2+ entry
2) Cell stimulated to make NO –> diffuse backwards
3) potentiates NT release (presynap cell release more NT quanta)
requires retrograde signal to presynaptic terminal –> more Ca thru NMDA –> NO –> potentiate NT release)
Pavlov’s experiment
Unconditioned response?
Conditioned response?
unconditioned = salivate when given meat
condition = salivate when hear bell
How is coincidence detection involved in Pavlov’s expeirment?
Unconditioned = sensory neuron in tongue innerv motor neuron to salivary gland –> salivation
Conditioned = b/c motor neuron also innerv by 4 weak inputs, these can be strengthened by paring bell (weak input) with meat (strong input) = COINCIDENCE
mechanism of coincidence detection in associative conditioning
1) ring bell –> release of glutamate at weak input
meat juice –> AP in motor neuron to depol enough to pop Mg out of NMDA on “ring bell” neuron
2) bell neuron now activated NMDA –> incr in AMPA receptors in bell presynap membrane
3) then now bell is sufficient to create AP –> salivation
By itself, just smelling cookies doesn’t produce a stimulus strong enough to produce an AP in the filling-out neuron. But every time the sensory neuron that senses spare time causes the filling-out neuron to depolarize to threshold AT THE SAME TIME THAT the cookie-sensor is releasing glutamate onto the same neuron (ie. whenever you sense both spare time and fresh cookies), the NMDA receptor right near the cookie-sensor synapse flips open (since the glutamate released from the cookie neuron activates its gate), the magnesium ion comes out (since the membrane is being depolarized by the spare time neuron), and calcium ions come into the postsynaptic membrane near the cookie synapse, making more AMPA ion channels insert themselves into that membrane. Due to these extra AMPA channels, the cookie neuron (but no others, since the AMPAs were only inserted next to the cookie synapse) has an increased ability to depolarize the LO neuron. If this process is repeated enough, eventually all you’ll have to do is smell fresh cookies and you’ll be filled with an uncontrollable urge to go fill out LOs while munching on them.
Note that in addition to inserting more AMPA receptors in the postsynaptic membrane, changes can also occur in the presynaptic neuron– the NMDA receptor can trigger release of nitric oxide (damn, we use it for everything), which drifts back across the synapse and makes the presynaptic terminal more able to release more vesicles at once. Same idea as the AMPA thing, just a different mechanism.
CNS neurons typically receive synaptic inputs
from many differnt neurons (many dendritic spines on to incoming axon terminal)
Difference btwn effect of CNS input vs muscle fiber NMJ
CNS = weak b/c 1 active zone with few vesicles and little NT/vesicle but postsyn cell weighs combined inputs from many individuals`
most common way of terminating transmitter action in CNS
Transporters to pump NT back into presynap terminal
Glial cells recycle
Diffusion
define synaptic integration
summation of excitatory and inhib potentials
Describe smart synapse
excitatory synapse
glutatamate NT
2 glut receptor = NMDA + AMPA
Describe silent synapse
some excitatory CNS synapses when stimulate evoke no change in postsyn cell
due to no AMPA receptor in postsyn cell but become functional when stim postsyn cell too
calcium incr through NMDA receptor causes
1) signaling cascade
2) incr in post syn receptor density due to protein translation
3) same # of transmitter molec have larger effect (potentiation)
