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Neural coding

TermDefinition
Spike encoding purpose Long/short neurons encode spike train to be appropriate to stimulus size
Axon w/ VGNaC and delayed rectifier K+ conductances encoding properties Depolarised by injecting steady current -> rate of firing depends on injected current magnitude -> all/nothing fire (no grading)
Depolarised cell neuron encoding properties Rate of AP firing is graded function of injected current -> encodes depolarising input as train of APs -> frequency depends on stimulus/synaptic potential magnitude -> requires further K+/different conductances (inactivates on maintained depolarisation)
What is the A current? K+ current inactivates themselves over time -> VG Ca2+ independent K+ currents -> rapid inactivation rates
VG A-type transient K+ channel opening Resting Vm -> inactivated, hyperpolarised -> removed inactivation, depolarised -> transient channel activation
Purpose of A current? K+ efflux -> prevents cell from becoming too depolarised -> delays onset of next burst -> spaces out APs in spike train
What is bursting? Periods of rapid AP spike -> long quiescent periods (longer than typical inter-spike intervals)
Where is bursting transmission found? CPG operation (pons breathing), neuropathologies (epilepsy), cortical pyramidal cells
Advantages of bursting transmission AP single spikes can only encode info in intervals (low fidelity) and are sensitive to noisy signals/mistimings, can encode info in specific shape of single burst, burst frequency encodes input intensity, intrinsic bursting has diverse role
Which cells have intrinsic bursting? Cells driven by constant subthreshold input -> complex feedback systems -> bursting patterns w/ less input dependence/sometimes in isolation
Neurophysiology of bursting? Slight depolarisation activates low threshold T Ca2+ channels -> Ca2+ influx -> spike firing (burst) continues as long as [Ca2+]i high -> elevated [Ca2+]i -> 2ndary messenger cascade -> promote Ca2+ efflux/Ca2+ channel inactivates -> rapid bursting ceases
Types of Ca2+ channels in neurons T (transient), L (long-lasting), N (neither), P (Purkinje)
T channel properties -65 mV threshold, brought to threshold by HCN4 -> inactivated by steady depolarisation for 20-50 ms -> rhythmic burst firing -> slow-wave sleep -> recovery during hyperpolarised Vm
L channel properties -20 mV threshold, inactivated for 500 ms -> synaptic transmission/dendritic Ca2+ spikes
N channel properties -20 mV threshold, inactvated for 50-80 ms -> synaptic transmission/dendritic Ca2+ spikes
P channel properties -50 mV -> dendritic Ca2+ spikes
What is tonic mode? Cell at more depolarised potentials (-58 mV) -> not sufficiently hyperpolarised to activate Ih -> T channels permanently inactivated -> relay neuron repeatedly fires single spikes instead of bursts
Postsynaptic neuron firing patterns Burst -> LTP, spike -> long-term depression
Burst synchronisation Aligned bursting in interconnected neurons (not necessarily w/ intrinsic bursting) -> synchronisation linked to plasticity/memory via Hebbian plasticity/LTP
What is responsible for spike frequency adaptation? Ca2+ activated K+ channels -> open with VGCaC influx -> K+ efflux opposes depolarisation -> slow spike firing/burst termination
What must sensory receptors be able to do? Capable of spiking during prolonged stimulation via coupled Ca2+/cAMP oscillation
Renshaw cell of spinal cord Stabilises motor neuron firing via feedback inhibition
What is post-tetanic potentiation? Repeatedly stimulated synapse varies transmitter release during stimulus train
What happens in nerves with repeated stimulation? Synaptic facilitation of postsynaptic potential -> progressive Ca2+ buildup w/in presynaptic terminal -> aid vesicle release
What happens in nerves with repeated tetanic stimulation? Synaptic depression -> depletion of readily-releasable vesicle pool
What happens in nerves when repeated tetanic stimulation ceases? Synapse recovers from depression -> more vesicles available due to previous synthesis for demand -> enhanced postsynaptic potential -> post-tetanic potentiation (minutes after tetanic stimulation ceases)
Experiment yielding long term potentiation Weak set tetanus -> transient post-tetanic potentiation but cell doesn't fire -> strong set tetanus -> cell fires but no weak contribution -> tetanic stimulus to both -> cell fires, both input EPSPs increase -> associative long-term potentiation
What is long term potentiation? Long-lasting excitability changes poststimulation -> follows Hebb's Law
What is Hebb's Law? Input strengthened when playing role in firing target cell -> A consistently excites cell B -> metabolic change/growth process in one/both cells -> A efficiency in firing B increases
Neurophysiology of LTP Released Glu opens NMDA -> Ca2+ influx works on CaM -> activate protein kinases/NO synthase -> increase postsynaptic AMPAR density -> long term changes in synaptic excitability
What is needed for LTP? Nt release and postsynaptic depolarisation
How is LTP maintained? Protein kinases autophosphorylate -> activate gene transcription/protein synthesis, opening of VGCaC
Cytoskeletal changes in LTP CaM kinase II neutralises +ve charge on stargzin protein coupled to AMPAR -> attaches AMPAR to PSD-95 protein -> provide additional AMPAR docking slots
What is long-term depression? Excitatory input fails to activate target neurons for postsynaptic potential causes specific synaptic depression
Neurophysiology of LTD Lower Ca2+ influx via NMDA R -> activate protein phosphatases -> remove phosphoates for LTP
Created by: vykleung
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