6- synap phys 2 Flashcards
What is mechanism that determines whether synapse is direct (fast) or indirect (slow)
examples of each
Fast = ionotropic (NT act directly on ion channel)
Slow = metabotropic (NT acts on GPCR and requires activ of 2nd messenger)
What is example of ionotropic and metabotropic mechanisms
ex = muscle fiber depol –> ACh bind nicotinic AChR –> open NSC channel –> Na+ enter –> muscle depol
ex = opening of K+ channel in heart
ACh bind muscarinic AChR –> activ GPCR –> gammaBeta released and diffuse to K+ channel –> open and K+ exits
What channel is opened in fast excitation? What is major NT involved?
What ions is permeable
major excitatory NT =glutamate and opens non-selective cation channel
permeable to Na and K
Na enter cell and depol
Define elctrical driving force
What is it the difference btwn
force to move ion across membrane (difference btwn voltage ion wants to be at (equilibrium) and actual membrane potential (Em))
Define reversal potential
Reversal potential = due to many NSC channels open –> membrane potential settle btwn ENa and Ek (~10 mV)
since greater than threshold –> therefore, excitatory and membrane depol
what kind of channel is opened during fast inhibition
main NT involved?
Which direction is the ion moving?
GABA
opens Cl channels in postsynap membrane
Cl- equilibrium potential more negative than threshold potential so Cl- movement does NOT CAUSE ACTION POTENTIAL
Why is inhibition more powerful than one might predict from size of an IPSP
b/c depends on relative permeabilities of ions
Small IPSP can reflect huge permeability change if ion’s equilibrium potential is close to resting membrane potential
Distinguish btwn temporal and spatial summation of postsynap potentials
When two diff presynap inputs synapse on a single neuron, potentails added to form larger potential since large amt of NT released
IF single input stim twice in succession, 2nd rise can start rising before previous AP has ended
Mechanism of synpatic transmission
1) AP arrives
2) open VG Ca2+ channel
3) Ca2+ bind synaptotagmin causing fusion of lipids of vesicles and surface membrane
4) open fusion pore to release NT (exocytosis)
5) NT bind receptors
Postsynaptic response depends on
nature of postsyn receptor
3 ways of removing NT
1) diffuse out of cleft
2) recycle by pump back to presyn terminal using Na coupled carrier molec
3) NT destroyed using extracellular degradative enzymes (ex = Ach)
How do you recycle the vesicle
1) vesicle membrane reinternalized (endocytosis) and filled with NT
2) NT synth locally and pump via Na coupled transporters into vesicle
Speed Effect Strength Transmitter Termination
of NMJ vs CNS synapses
fast vs. (fast or slow)
excitatory vs (excit or inhib)
strong vs weak
Ach vs many others (Ach, glu, GABA, 5-HT, DA, Asp…)
diffusion/degradation by esterase (reuptake) vs. reuptake or diffusion (degradation)
difference btwn postsyn membrane in skeletal vs. neuron
skeletal = many folds to incr density of NT receptors
Motor unit define
NT in motor synapses with muscle
motor unit = axon + muscle fibers
NT = ACh
Ach receptor is what type of channel
ligand gated ion channel (binding of Ach stim open gate and influx of Na to depol)
what type of channel is ACh
NSC (permeable to all cations)
components of ACh receptor
4 subunits (2A, B, C, D) around pore each A binds one ACh and must bind simult
how to clear Ca from synapse
2 channels
1) ATP driven
2) Na/Ca exchanger
What happens if ECl is equal to resting membrane potential
IPSP amplitude = 0 but would still be inhibitory on EPSP
What happens when the NT causes a decr in K+ ion permeability
depolarized bc excitatory synapse
Describe presynaptic inhibiton
inhib nerve terminal synape on excitatory presynap terminals
–> inhib release GABA –> open Cl in presynap cell –> decr Ca2+ ch, less excitatory NT release
shuts off input to cell without affect cell’s resting membrane potential or synaptic effect of other input
Suppose a single excitatory input was stimulated twice in succession. The first EPSP was 10 mV in amplitude, and lasted 20 msec. The second stimulus was given 50 msec after the first, and the EPSP was 15 mV. Was the larger size due to facilitation or summation or both?
facilitation, of course, because the first EPSP had completely decayed before the second stimulus was given
suppose the second stimulus in the example above was given only 10 msec after the first, and the peak of the EPSP was 15 mV.
temporal summation - it arises when the same input stimulated in succession.
benefit of indirect over direct synaptic transmission
NT in cleft longer –> extended action after NT action finished (ex= emotion)
2nd messengers transmit chemical signals to nucleus –> change gene expression
example of first messenger doing double duty turning on fast and slow (direct/indirect)
autonomci ganglion receive cholinergic input from CNS –> ACh release –> ionotropic in NMJ –> NSC that depol
ACh activ metabotropic receptor in postsyn –> slower depol by closing K+ channels
2 types of ACh receptors
agonist and antagonist
nictoinic ACh receptor
agonist = nicotine
antagonist = curare
muscarinic ACh receptor (GPCR)
agonist = muscarine
antagonist = atropine
Define
Neostigmine
Curare (d-tubocurarine)
blocks ach esterase and prolongs current at NMJ (used for myasthenia gravis/syndrome)
Curare = block ACh receptor and induces paralysis; relaxant in anesthesia
