Synaptic Physiology I-III Flashcards Preview

Nervous System: Unit I > Synaptic Physiology I-III > Flashcards

Flashcards in Synaptic Physiology I-III Deck (29)
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1
Q

Action potential mechanism

A
  • Na+ channel gate is triggered to open via stretch/other stimulus
  • Na+ flows in ==> membrane depolarization
  • Voltage-gated Na+ channels open ==> increased Na+ flow inwards
    • Action potential will occur completely if membrane reaches threshold potential
  • Inactivation gates begin to close on voltage-gated Na+ channels ==> slowing of Na+ flow
  • K+ channels open ==> K+ flows out of cell ==> cell repolarizes
  • Ion channels reset to resting position & Na/K transporter helps restore resting membrane potential
2
Q

Electric synaptic transmission definition/characteristics

A
  • Gap junctions allow direct passage of electrical signal between cells
  • Rare in nervous system of mammals
    • Chemical synaptic transmission dominates the nervous system
  • Important in fxning of heart, smooth muscle, embryonic cells, and epithelia
3
Q

Major limitation of electrical vs. chemical synaptic transmission

A
  • presynaptic terminal must be comparable in size to postsynaptic cell in order to provide enough current to depolarize the cell
    • would not fxn @ a neuromuscular jxn b/c the current generated by the much smaller neuron would not generate enough depolarization @ muscle
  • electric transmission is by default excitatory ==> more difficult to integrate excitatory and inhibitory synpatic inputs as is achieved at chemical synapses
4
Q

Mechanism of NT release at the presynaptic cell

A
  • AP reaches the end of the cell (“active zone”)
    • Active zone ECa = +120mV b/c the concentration of Ca2+ is significantly higher outside the cell
  • Ca2+ channels open ==> Ca2+ flows in quickly
  • Ca2+ attaches to vesicles containing NTs via SNARE proteins ==> fusion of vesicle to cell
  • NTs escape into the synaptic cleft
5
Q

SNARE proteins involved in NT release

A
  • Located on NT vesicles:
    • Synaptotagmin
    • Synaptobrevin
  • Located on surface membrane:
    • Syntaxin
    • SNAP-25
6
Q

Mechanism of SNARE-mediated vesicle fusion

A
  • Ca2+ attaches to synaptotagmin (located on vesicle)
  • Synaptobrevin, syntaxin, and SNAP-25 form a super-helix used to fuse with the membrane
  • Vesicle fuses with membrane and NTs are released into the synaptic cleft
7
Q

Presynaptic events involved in cleanup/recycling (occuring outside the cells)

A
  • reuptake: pumps bring NTs back into the cell for reuse
  • degradation: e.g. AChE ==> acetate + choline
  • diffusion into ECF
8
Q

Presynaptic events involved in cleanup/recycling (occuring inside the cells)

A
  • Na/K pump: restores sodium/potassium ion balance
  • ATP & NCX pumps: calcium exchanger helps restore calcium ion balance
  • Endocytosis of vesicles
    • clathrin + clathrin adapter induce the reformation of vesicles
    • dynamin (“pinch-ase”) separates the vesicle from the membrane
    • vesicle loses its coating and is refilled with NTs
9
Q

Major function of motor nerve terminal

A
  • AP from CNS ==> enough ACh to depolarize muscle fiber to threshold for AP
  • Muscle fiber resting = -80mV & threshold = -50mV ==> enough ACh to depolarize muscle by at least 30mV
10
Q

Mechanism of signal amplification @ NMJ

A
  • Synaptic vesicle contains thousands of ACh mlx ==> ~half consumed by AChE + 2ACh/receptor ==> activation of >1000 postsynaptic ACh receptors
    • each receptor ==> 1000nV of positive charge = 1microV
    • 1000 x 1microvolt = ~1mV/vesicle
  • Need @ least ~30 vesicles to reach threshold
  • 1 AP ==> 100 quanta (vesicles) in order to maintain sustained muscle use
  • Amplification accomplished by releasing a large amount of NTs for each AP
11
Q

Facilitation & Depression of NT release (definition)

A
  • During repetitive nerve stimulation…
  • facilitation = calcium ion concetration builds up
  • depression = pool of releasable vesicles is depleted
12
Q

Mechanism of facilitation of NT release

A
  • Ca2+ concentration @ terminal rises during h_igh frequency stimulation_ b/c there is not enough time to restore Ca2+ balance
  • Exocytosis depends on Ca2+, therefore number of quanta released will increase due to residual Ca2+
13
Q

Mechanism of depression of NT release

A
  • repetitive stimulation ==> nerve terminal runs out releasable vesicles
    • terminal cannot replenish synaptic vesicles from reserve pool fast enough to meet demand
  • Exocytosis depends on supply of synaptic vesicles, therefore number of quanta released will decrease
14
Q

Myasthenic syndrome characteristics

A
  • Ab againsts Ca2+ channels
  • Characteristically weak, but can fire APs @ muscle & improve strength with effort
    • relies on facilitation to build up enough Ca2+ to release enough NTs to generate APs @ muscle
15
Q

Myasthenia gravis characteristics

A
  • Disease w/Abs against AChR ==> initial strength is good, but tire very quickly
    • With fewer postsynaptic AChR, M.G. people generally need to release more quanta to fire APs
    • Due to synaptic depression (reduction of 10% of available quanta/AP), M.G. people quickly fall below the required number of quanta to fire APs @ muscle
16
Q

Mechanism of fast vs. slow synapses (e.g. of physiologic responses)

A
  • determined by type of receptor on the postsynaptic cell
  • fast = direct = ligand/ion-gated channel
    • e.g. muscle contraction
  • slow = indirect = g-protein-coupled receptors
    • e.g. emotion
17
Q

Characteristics of fast channels

A
  • selective = allows a single type of ion
    • Na+ selective = excitatory
    • K+ selective = inhibitory
  • non-selective = allows both Na+ and K+ to flow across
    • fastest-acting channel
    • ending membrane potential will rise above level needed to depolarize
18
Q

Characteristics of slow channels

A
  • Slow receptors act indirectly ==> no channel is opening upon binding to receptor
  • Slow receptors couple w/g-proteins and/or 2nd messenger systems
  • NT binds to receptor ==> activation of g-protein/2nd messenger ==> reaction w/in cell:
    • e.g. opening of a separate channel (temporary)
    • e.g. effector entering nucleus to alter gene transcription (permanent/semi-permanent)
19
Q

Electrical “driving force” definition

A
  • difference between membrane potential and equilibrium potential of a particular ion ==> induces flow across the membrane if physically permitted
20
Q

Characteristics of synaptic reversal potential

A
  • NSC (Non-selective cation) channel is permeable to both Na+ and K+ ==> brings membrane potential to value midway between ENa & EK ==> “synaptic reversal potential”
    • AChR @ NMJs operate in this way
  • Reversal potential for NSC channels = -10mV which >-55mV ==> these channels are excitatory
21
Q

Channels involved during fast inhibition @ CNS

A
  • GABA binding induces opening of Cl- channels
22
Q

Mechanism of amplified strength of individual IPSP

A
  • **Membrane potential is determined by relative permeabilities of all participating ions
  • IPSP @ 1mV ==> huge permeability change if ion’s equilibrium potential is near resting potential ==> ECl ~ E0
23
Q

Spatial and temporal summation of postsynaptic potentials (definition)

A
  • spatial summation = two or more different inputs contribute
    • e.g. various excitatory inputs coverge on a motor neuron fire simultaneously ==> combine (“summate”) to drive membrane potential to threshold for AP
  • temporal summation = same input is stimulated multiple times in succession
24
Q

Mechanisms for removing NTs from synaptic clefts

A
  • reuptake: pumps bring NTs back into the cell for reuse
  • degradation: e.g. AChE ==> acetate + choline
  • diffusion into ECF
25
Q

Generic types of dendritic receptors

A
  • NMDA receptors
  • AMPA receptors
26
Q

Coincidence detector characteristics

A
  • Major criteria for coincidence detector:
    • can detect the presence of NT in cleft
    • can detect change in membrane potential
  • Coincidence detectors = key for associative learning
    • “make synapses smart”
  • e.g.: NMDA receptor
27
Q

Calcium impact on postsynaptic dendrites @ CNS

A
  • Calcium induces vesicles w/AMPA receptors to fuse with membrane
  • Increased AMPA receptors @ surface ==> next synapse firing = larger postsynaptic response
28
Q

Mechanism of coincidence detector via NMDA receptor

A
  • NMDA opens in presence of presynaptic NTs + APs generated at a different dendrite/location in the neuron
    • NMDA pore is plugged by Mg2+ @ rest
    • NMDA channel gate is opened by the presence of glutamate (NT presence)
    • Mg2+ is repelled in presence of positive charge (firing of AP), allowing Ca2+ to enter cell
  • ​If an AP occurs + NT release at the presynaptic neuron ==> open NMDA channels ==> Ca2+ influx ==> increased AMPA channels ==> stronger connection w/presynaptic neuron
29
Q
A