MODULE 3- Synaptic Transmission Flashcards
2 mechanisms of synaptic signaling
-chemical synapses
-electrical synapses
chemical synapses
use neurotransmitters + their receptors
-Ca2+ dependent neurotransmitter release
chemical synapses are unidirectional/bidirectional
unidirectional
chemical synapses are slow/fast
slow
chemical synapses- what do ions flow through
postsynaptic channels
electrical synapses
use gap junctions as ion channels
electrical synapses are unidirectional/bidirectional
bidirectional
electrical synapses are slow/fast
fast
electrical synapses- what do ions (current) flow through
connexon channels
synaptic delay between 2 cells at electrical synapses
less than 0.1 msec
hippocampal interneurons
one of the few places in the CNS that use electrical synapses
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
electrical synapses- what happens as current sweeps across tissue
entire tissue can be stimulated virtually simultaneously as the current sweeps across it
key hallmark feature of chemical synapses
use of a chemical neurotransmitter
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
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
co-transmitters
sometimes a neuron can synthesize + release more than 1 type of neurotransmitter
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
what do calcium ions regulate
the release of discrete packets of neurotransmitters
what does synaptic transmission at the NMJ result in
end-plate potentials (EPPs)
what do spontaneous firings in the muscle cell result in
miniature EPPs (MEPPs)
what is equivalent to a MEPP
ACh released in discrete packets
what do EPPs represent
many simultaneous MEPP-like units
train of presynaptic APs causes what
rise in Ca2+
-tracked by Ca2+ dependent fluorescent dye
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
