Neural coding Word Scramble
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| Term | Definition |
| 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 |
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vykleung
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