Synaptic transmission 2 Flashcards
describe magnesium experiment setup
single neuromuscular junction (neuron + muscle fibre) was isolated
ca2+ in ecf was replaced by Mg2+, which can’t enter cells as easily. therefore, fewer vesicles would be released, allowing us to measure the EPSP of a few vesicles at a time.
axon stimulated, muscle membrane potential recorded.
describe magnesium experiment results
- no response
- differing responses
- spontaneous release of vesicles (didn’t require stimulation)
how were results of magnesium experiment recorded?
histograms
describe miniature end plate potential
potential difference caused by the release of ONE vesicle
do each vesicles contain a similar amount of nt, and produce a similar PSP?
yes
main mode of conduction in dendrites?
mainly passive.
also active, but not the same as action potentials - don’t depolarise the membrane as much, and are less reliable.
describe how passive conduction occurs in dendrites.
current is injected; ions diffuse bidirectionally through open channels
strength of current decays exponentially.
what constant is used to quantify passive conduction?
length constant: distance at which depolarisation decays to 1/e of maximumsize
factors affecting length consant?
internal resistance: diameter
membrane resistance: density of open channels
what mechanism is used to counteract the fact that EPSPS decay along the dendrite?
distal synapses produce larger EPSPs than proximal (closer to axon hillock) synapses
Ecl- =
-65mV = resting membrane potential
how are chloride channels opened
GABA binds to them
two ways in which chlorie channels mediate inhibition?
mathematically summing with EPSPs
shunting inhibition
describe shunting inhibition
Inhibitory (GABA) axo-somatic synapses open chloride channels. This allows charge leakage, preventing EPSP from reaching the cell body
ways in which we can modulate the probability of vesicle release (hence strength of EPSP)?
presynaptic modulation presynaptic faciliation paired pulse faciliation autoreceptors astrocytes
describe presynaptic modulation
axo-axonic synapses regulated ca2+ entry into axon terminal (hence modulate vesicle release)
when the synapse is active, it reduces amount of ca2+ going into the cell, reducing number of vesciles released…
describe presynaptic facilitation
when the axo-axonic synapse is activated, allows more Ca2+ to enter the cell
describe paired pulse faciliation
when second AP arrives, ca2+ might be left over from first AP.
therefore, even more vesicles may be released, so therefore current will increase
depends on temporal summation
describe autoreceptors
presynaptic metabotropic receptors which regulate that neuron’s level of nt release
- too much nt in cleft: reduces synthesis and release of nt
- too little: increases nt release
- changes reuptake accordingly
describe how astrocytes work
uptake nt’s from synaptic cleft
release substances into synaptic cleft to promote nt release
describe temporal summation dependency on time consatn
long time constant: repolarisation slower. so second synaptic current adds onto it, resulting in a high synaptic potential
short time constnat: repolarisation quicker; so second synaptic current doesn’t add onto it, resulting in lower synaptic potential
describe spatial summation dependency on length constant
as previous
