Ionic mechanisms Flashcards
What happens when you block potassium channels with TEA… and WHY
impair firing + broaden ap
there is less driving force - Na channels cannot recover completely from inactivation because mempot is not negative enough
What does the Beta subunit do
is can turn non-inactivating delayed rectifiers into inactivating channels by co-expression of beta subunit
What happens to aps when Kv channels are inactivated
prolong ap duration
cumulative inactivation of Kv channels = decreased repol and spike broadening
What are LVA currents and there function
low voltage currents require negative resting potential
lva ca2+ channels are available at -65mV in neurons that act slowly and cause a wave like depolarisation of the resting potential
how to monitor intracellular Ca2+
Ca2+ sensitive fluoro markers = aequorin bind to Ca2+ and emits blue light
then green fluoro protein absorbs blue light and emits green
What sets neuronal firing patterns
slow Cav + Kca channels
excitatory + inhibitory channels create fast and slow components of firing patterns
What is required for rhythmic bursting
Nav + Kv + Cav + Kca
What is accommodation and how can it be overcome
channels react to a change then adapt
is reversed after noradrenaline (decrease Kca current) because sympathetic stimulation = neuons maintain sustained activity
Describe phosphorylation of Kca channel regulation
GPCR signalling - noradrenaline - synthesise cAMP - activate protein kinase A (PKA)
decrease open probability of Kca and decrease sensitivity to Ca and V stimuli
therefore accommodation depends on Kca act
describe how we know that Kca + Cav are colocalised on cell membranes
patch clamps + prepulse
+80 without a prepulse = low Ca activity
+80 with -20mV prepulse = increase ca and Kca entry
+80 with +80 prepulse = no driving force
no increase in current without a prepulse, and fast K currents with prepulse indicates that they are colocated
functions of fast Cav + Kca channels
shape ap repol
ca entry activated Kca entry
late phase ap is delayed with Kca blocker
how does ap affect ca release
ca entry produce locally high concentrations of Ca and synaptotagmins will mediate vesicle entry
duration and frequency of ap will influence ca entry at the presynaptic terminal and then regualte the types of ntsm release
what is the difference between releasine small molecule chemical transmitters and neuropeptides
neuropeptides release from deep-core vesicles require broad aps, and high IC ca (long + slow responses)
small molecule ntsm release requires small IC Ca = immediate effects (fast EPSPs + IPSPs)
the Ca plateau is counterbalanced by BK current
8
