Neurotransmitters Flashcards
How are electrophysiological & microscopy techniques can be used to investigate the release
of neurotransmitter at a synapse?
Recording miniature end plate potential (mepps) at the NMJ.
Electron microscope (EM) studies reveal vesicles at the synapse in the apparent act of exocytosis.
Describe key experiments used to investigate the role of vesicles in neurotransmitter release
The number of pits in the membrane were measured, this shows the number of fusions with the membrane have taken place.
Drug 4-AP acts by blocking potassium channels, prolonging action potentials and thereby increasing neurotransmitter release at the neuromuscular junction
As the concentration of 4-AP drug increases, transmitter packets released increases, the pit number increases, more and more fusions occur.
What is the role of key synaptic proteins in neurotransmitter release?
x
how are the effects of particular drugs &
toxins on synaptic transmission determined?
On examination of varing amplitude of toxin mepp against control mepps.
Describe synaptic transmission.
1) Action potential received.
2) Ca2+ influx into the cell via Ca2+ channels.
3) Vesicular transmitter release from cell.
4) Activation of transmitter-gated ion channels on post synaptic receptor.
5) Activation of voltage-gated ion channels.
What family does the nAChR belong to?
It is a transmitter-gated ion channel belonging to the cys-loop superfamily which mediates fast synaptic transmission (in milliseconds) of SELECTIVE IONS
nAChR is located in the brain and nervous system.
Undergoes a conformational change of its 5 subunits when channel is open in response to an agonist.
What do mepps represent?
represent little packets of ACh being released (causing depolarisation)
What is the effect of VESAMICOL?
It inhibits vesicular uptake of ACh and then consequently DECREASES the amplitude of mepps
decrease amount of ACh released in the vesicle in the first place.
What is the effect of alpha-Latrotoxin (BLACK WIDOW VENOM)?
First, exocytosis is encouraged, and EXCESS ACh is released causing muscle spasms due to countless mepps.
Then, reforming vesicles (endocytosis) is distrupted and therefore no mepps, no muscle stimulation and paralysis.
What is a quanta? How does it lead to muscle contraction?
A packet of transmitter, ie, a single vesicle gives a single Quanta
This activated a ACh receptor which in turn gives rise to a single mepp.
Single mepps add up and make a overall epp which produces an A.P
if A.p is large enough, muscle contracts.
What are the advantages of having a specialised membrane for vesicle production?
It allows recycling of vesicles or economic reasons; they are reformed in endocytosis befor undergoing exocytosis once more.
How do the microdomains of Ca2+ concentrations show neurotransmitter release.
A.P depend on Ca influx into the cell.
The neurotransmitter is stimulated by an A.P in which calcium and a vesicle are cycled each time.
Calcium levels high (800micromoles) before vesicle release, and fall dramatically (25micromoles) after its release.
Indeed if calcium levels are too low on the OUTSIDE of the cell, there is not enough to make an action potential (blow threshold.) and channel doesnt open
Explain the statement “Release of neurotransmitter at the NMJ is quantal”
Number of vesicles released is proportional to the amplitude of the epp (A.P) produced.
One packet/vesicle has a smaller epp than the epp produced by the reception of 4 vesicles.
What is a mEPSP in glutamate receptors?
CNS, glutamate receptor mediated miniature excitatory postsynaptic potentials (mEPSPs) summate to produce an EPSP and lead to neuronal excitation.
What is an IPSP in GABAA receptors?
GABAA receptor mediated miniature inhibitory postsynaptic potentials summate to produce an IPSP and lead to neuronal inhibition.
