MODULE 3- Synaptic Transmission Flashcards by Tara Track

2 mechanisms of synaptic signaling

-chemical synapses
-electrical synapses

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chemical synapses

use neurotransmitters + their receptors
-Ca2+ dependent neurotransmitter release

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chemical synapses are unidirectional/bidirectional

unidirectional

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chemical synapses are slow/fast

slow

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chemical synapses- what do ions flow through

postsynaptic channels

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electrical synapses

use gap junctions as ion channels

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electrical synapses are unidirectional/bidirectional

bidirectional

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electrical synapses are slow/fast

fast

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electrical synapses- what do ions (current) flow through

connexon channels

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synaptic delay between 2 cells at electrical synapses

less than 0.1 msec

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hippocampal interneurons

one of the few places in the CNS that use electrical synapses

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due to the bidirectional transmission of electrical synapses, generation of APs in one neuron results in what

synchronized firing of APs in the adjacent neuron

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electrical synapses- what happens as current sweeps across tissue

entire tissue can be stimulated virtually simultaneously as the current sweeps across it

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key hallmark feature of chemical synapses

use of a chemical neurotransmitter

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ultimately, what is the AP in the postsynaptic neuron generated by

the opening of ion channels
-which changes the membrane potential
-achieved through either ionotropic or metabotropic receptors

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3 criteria of a neurotransmitter

-must be present in the presynaptic neuron
-must be released during synaptic activity
-must bind receptors on the postsynaptic neuron

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co-transmitters

sometimes a neuron can synthesize + release more than 1 type of neurotransmitter

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steps of a chemical synapse

transmitter is synthesized + then stored in vesicles ->

an AP invades the presynaptic terminal ->

depolarization of presynaptic terminal causes opening of voltage-gated Ca2+ channels ->

influx of Ca2+ through channels ->

Ca2+ causes vesicles to fuse with presynaptic membrane ->

transmitter is released into synaptic cleft via exocytosis ->

transmitter binds to receptor molecules in postsynaptic membrane ->

opening or closing of postsynaptic channels ->

postsynaptic current causes excitatory or inhibitory postsynaptic potential that changes the excitability of the postsynaptic cell ->

removal of neurotransmitter by glial uptake or enzymatic degradation ->

retrieval of vesicular membrane from plasma membrane

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what do calcium ions regulate

the release of discrete packets of neurotransmitters

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what does synaptic transmission at the NMJ result in

end-plate potentials (EPPs)

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what do spontaneous firings in the muscle cell result in

miniature EPPs (MEPPs)

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what is equivalent to a MEPP

ACh released in discrete packets

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what do EPPs represent

many simultaneous MEPP-like units

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train of presynaptic APs causes what

rise in Ca2+
-tracked by Ca2+ dependent fluorescent dye

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what does microinjection of Ca2+ chelator into presynaptic terminal prevent

prevents transmitter release + therefore postsynaptic APs

what does increasing presynaptic [Ca2+] do

causes neurotransmitter release from presynaptic terminals

what is responsible for neurotransmitter release

a cycle of membrane trafficking

quantal release of neurotransmitters

-individual quanta of neurotransmitters are caused by the fusion of the vesicle memrbane with the plasma membrane -number of quanta released is positively correlated with the number of vesicles fusing

average synaptic vesicle diameter

~ 50 nm -corresponding to 100 mM of ACh

myasthenic syndromes affect which terminal

presynaptic

myasthenic syndromes

abnormal transmission at neuromuscular synapses -leads to weakness + fatigue at skeletal muscles

what 3 things can myasthenic syndromes affect

-acetylcholinesterase -cholinergic receptors -voltage-gated Ca2+ channels (VGCC)

Lambert-Eaton myasthenic syndrome

loss of VGCCs (voltage-gated Ca2+ channels)

myasthenia gravis

an autoimmune disease that produces antibodies against nicotininc ACh receptors at the NMJ -produces weakness + fatigue -produces much smaller EPPs + MEPPs than in unaffected people

how can myasthenia gravis be improved

with acetylcholinesterase inhibitors, such as neostigmine -this would increase the concentration of ACh in the synapse

what is the "protocol neurotransmitter"

ACh

what was the 1st neurotransmitter to be discovered

ACh

**what is ACh derived from

-acetyl-CoA -choline

**what does acetylcholinesterase metabolize ACh into

-acetate -choline

acetylcholinesterase efficiency

extremely efficient -5,000 ACh metabolized per second

2 families of neurotransmitter receptors

-ligand-gated ion channels -metabotropic receptors

ligand-gated ion channels are also called

ionotropic receptors

ligand-gated ion channels (ionotropic receptors)

receptor itself is also the ion channel

ligand-gated ion channels (ionotropic receptors) are slow/fast

fast -postsynaptic potentials responses range 1-2 msec after an AP reaches the presynaptic terminal

metabotropic receptors are also called

G-protein-coupled receptors

metabotropic receptors (G-protein-coupled receptors)

G-protein complex is activated by ligand binding to the receptor

metabotropic receptors (G-protein-coupled receptors) are slow/fast

slow -postsynaptic potentials responses range from hundreds of msec to 1-2 min

steps of ligand-gated ion channels

neurotransmitter binds -> channel opens -> ions flow across membrane

steps of metabotropic receptors

neurotransmitter binds -> G-protein is activated -> G-protein subunits or intracellular messengers modulate ion channels -> ion channel opens -> ions flow across membrane

what changes during synaptic transmission

postsynaptic membrane permeability

what opens ligand-gated ion channels when binding to its receptors

ACh

end-plate current (EPC)

results when thousands of ACh receptors are opened as a result of the ligand binding to the former

EPC is an inward/outward current

inward current -causing a depolarization or postsynaptic AP -caused by the influx of Na+ and subsequent efflux of K+

what is EPC caused by

influx of Na+ and subsequent efflux of K+

**reversal potential (E rev)

the voltage at which direction of the current changes from outward to inward

what does reversal potential (E rev) reveal

the identity of the ions pemeating the postsynaptic receptors

what is reflected by the reversal potential of the EPC

permeability to any particular ion -would be at the equilibrium potential for that ion

describe permeability of ACh-activated ion channels compared to Na+ and K+

ACh-activated channels are almost EQUALLY permeable to both Na+ and K+ -shown by the findings that EPCs reverse at 0 mV

what do postsynaptic ion fluxes determine

determine whether synapses are excitatory or inhibitory

**excitatory postsynaptic potentials (EPSPs)

increase the likelihood of a postsynaptic AP

glutamate is an EPSP/IPSP

EPSP

EPSPs allow for influx of what ion

Na+ influx

inhibitory postsynaptic potentials (IPSPs)

decrease the likelihood of a postsynaptic AP

GABA is an IPSP/EPSP

IPSP

IPSPs allow for the influx + efflux of which ions

either Cl- influx or K+ efflux

EPSPs have ____ strength

subthreshold strength -not enough to generate an AP

IPSPs of equal subthreshold strength can do what to an EPSP

cancel out EPSP

what happens to all converging EPSPs + IPSPs stimulating a postsynaptic neuron

added together in both space + time

summation of synaptic potentials- space

how far away are each of them (synapse) from the axon hillock?

summation of synaptic potentials- time

how long does it take each PSP to reach the axon hillock?

if the combined strength (in mV) of PSPs reaches threshold...

an AP will fire + be transmitted down the axon

what does convergence of hundreds or thousands of presynaptic inputs across the soma + dendritic spines lead to

summation

as a result of summation across space + time, what do changes in membrane potential depend on

whether it reaches threshold

overview of postsynaptic signaling

neurotransmitter release -> receptor binding -> ion channels open or close -> conductance change causes current flow -> postsynaptic potential changes -> postsynaptic cells excited or inhibited -> summation determines whether or not an AP occurs