Modulation of synaptic transmission Flashcards
What are the two classes of ntsm
small molecule (ligang + gpcr) neuropeptide (gpcr)
describe the production of small molecule ntsm
enzymes synthesised in cell body, tansported via axons, synthesise and package ntsm and release and diffuse at terminal
fast synaptic transmission
describe the production of neuropeptides
synthesise precursors and enzymes in cell body
transport ex and prepeptides through microtubule tracks where ez modify pre peptides into ntsm
diffuse and degraded by proteolytic enzymes
modulate ongoing activity
describe the signalling mechanism of gpcrs
GDP contains alpha , beta, gamma
when gdp -> gtp, beta and gamma dissociate and diffuse into the cell
how do patch clamps detect gpcr activity
with a whole cell patch, we can tell that adrenaline activates Cav channels through GPCRs because it can modify channel current without going through pipette
What can noradrenaline do
can decrease or increase ap duration, depending on signalling pathway
What is the mechanism of NA in inhibiting Ca channels
NA -> PKA -? IP3 + DAG -> IP3 activate Ca stores -> protein kinase C will phosphorylate channel and decrease Ca2+ to decrease ap
Describe the feedback control mechanism of GPCRs
NA via GPCRs to control ntsm release in sympathetic neurons
decreases open probability for presynaptic Cav to decrease ntsm release
the downregulation is enabled by autoreceptors
How are inward rectifiers regulates and what function do they control
GPCR that respond to neuropeptides
affect mental state and cognitive function
differences between KV and Kir
2 separate families
Kv = 6 trransmembrane domains
Kir = only 5th and 6th
explain current in relation to Kir
inward current better than outward current
but meant for small outward currents which give the cell better control
when the mempot increases, the Kir set -ve memport
how is magnesium involved with Kirs
voltage sensitivity
positive potential = blocks channel with mg2+
negative potential = unblock
how are Kirs regulated
neuropeptide signalling
substance P is released with Ach for slow excitation (attention, arousal, motivation)
increases excitability by decreasing Kir
what does the phrenic nerve do
main control for diaphragm and intercostal muscles
what do the brainstem nuclei have to do with respiration
pre-botzinger complex has interneurons that set rhythmic firing
repetitive bursting using LVA, Kca, Nav, Kv
