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Neurons
| Question | Answer |
|---|---|
| Hippocampal pyramidal cell features | Pyramidal/conic body, 1 apical dendrite w/ multiple spines, multiple basal dendrites on soma, axon hillock, Glu/GABA nt |
| Dorsal root ganglion features | Pseudo-unipolar, soma offset from axon w/ distal/proximal processes |
| Retinal bipolar cell features | Soma within 2 processes, lie between photoreceptors/GCs, communicate via graded potentials (not APs) |
| Spinal motor neuron features | Soma in ventral horn of spinal cord w/ multiple dendrites, single axon projects to/outside spinal cord, long axon -> effector organs |
| Cerebellar Purkinje cell features | GABAergic inhibitory neurons, elaborate dendritic arbor w/ multiple dendritic spines, parallel fibres connect dendritic spines, store signal trajectory information |
| Na+ ion distribution | 15 mM in, 150 mM out, +60 mV, inward current |
| K+ ion distribution | 150 mM in, 5.5 mM out, -89 mV, outward current |
| Cl- ion distribution | 9 mM in, 125 mM out, -71 mV, inward current |
| Ca2+ ion distribution | 0.0001 mM in, 1 mM out, +124 mV, inward current |
| What maintains the Na+/K+ gradients? | Na+/K+ ATPase |
| Nernst equation purpose | Describes eqbm potential if membrane is permeable to that ion only |
| Nernst equation | E = RT/zF log ([out]/[in]) |
| Nernst equation exception | Cl- -> [in]/[out] |
| What is the resting potential? | -70 mV |
| Why is the resting potential? | Membrane principally permeable to K+ -> -70 mV close to K+ Nernst potential (-89 mV) |
| Donnan product rule | [K+]o x [Cl-]o = [Cl-]i x [K+]i |
| Donnan product rule rationale | Cl- Nernst ~ resting potential ~ K+ Nernst -> Cl- passively distributed and Ek = Ecl |
| How is Cl- extruded from cells? | K+/2Cl- cotransporter -> driven by Na+/K+ ATPase, Na+/HCO3-/H+/Cl- exchanger -> (HCl out) driven by Ca2+/H+ ATPase exchanger |
| Effect of Cl- extrusion | Lowers [Cl-]i -> Ecl more -ve than resting potential -> cell internal -ve charge contributed by other -ve macromolecules |
| How is Cl- moved in developing neurons/adult olfactory receptor neurons | Inward NKCC cotransporter -> raises [Cl-]i -> Cl- channel opens at resting potential -> excitatory Cl- efflux -> depolarises cell for spontaneous activity btwn interconnected neurons |
| How is Ca2+ extruded from cells? | Ca2+/2H+ ATPase, PMCA -> plasma membrane, NCX (Ca2+/3Na+) -> cardiac muscle, NCKX (Ca2+/K+/4Na+ in) -> retina |
| Effect of Ca2+ extrusion | Lowers [Ca2+]i < 0.0001 mM -> Ca2+ used as intracellular 2ndary messenger -> small Ca2+ fluxes have large influence on [Ca2+]i |
| Gap junction advantages | Free passage of ions/small molecules |
| Gap junction disdavantages | Large presynaptic terminal -> sufficient current to produce EPP, cells must be similar size/properties, bidirectional, inflexible communication |
| Where are gap junctions used? | Synchronised large cell population activity -> developing embryo, cardiac myocyte intercalated discs |
| Chemical synapse advantages | No size/voltage requirements, small cells rely on nt to produce EPP, unidirectional, flexible -> diffrent nt/receptors for excitatory/inhibitory |
| Chemical synapse disadvantages | Specific ions only transmit under correct conditions |
| Where are chemical synapses used? | Unidirectional signal transmission -> sensory neuron, motor neuron |
| Synaptotagmin | v-SNARE -> vesicular Ca2+ sensor |
| Synaptobrevin | v-SNARE -> aids fusion |
| Syntaxin | t-SNARE -> bind synaptotagmin in Ca2+ dependent manner |
| SNAP-25 | t-SNARE -> bind synaptobrevin |
| SNARE complex | Synaptobrevin, syntaxin, 2 SNAP-25 alpha helices |
| Vesicle fusion process | Docking at presynaptic active zone (weakly Ca2+ dependent), priming via SNARE proteins (membranes partially fused via fusion scaffold), fusion (Ca2+ dependent) -> exocytosis of nt |
| What influences vesicle fusion? | [Ca2+]4 e |
| Nt characteristics | Present w/in presynaptic terminal/synthesis mechanisms exist, released in adequate quantity on stimulation, added nt has same effect (stimulation/inhibition) |
| Ionotropic responses | Ion flow, fast excitation |
| Metabotropic receptors | 2ndary messenger cascades, modulate membrane conductance, slow/sustained effects |
| NMDA receptor | Glu receptor -> Mg2+ ion blocks pore at rest -> membrane depolarisation repels Mg2+ ion -> allows Na2+/Ca2+ influx -> slow depolarisation |
| non-NMDA receptors | AMPA, kainate receptors |
| AMPA receptor | Glu receptor -> Na+ influx, PO43- AMPA R can regulate channel localisation/conductance/open probability -> linear I/V relationship -> fast depolarisation |
| Major CNS excitatory transmitter | Glu |
| Major CNS inhibitory transmitter | GABA (brain), Gly (spinal cord) |
| GABA A receptor | Neurons/leydig cells -> Cl- efflux (excitatory)/Cl- influx (inhibitory), mediate shunting inhibition -> reduce cell excitability -> reduces depolarisation from concurrent signal |
| GABA B receptor | CNS/PNS autonomic division -> Gi/o coupled -> GIRK activation -> hyperpolarising K+ efflux -> reduce AP frequency/nt release |
| GABA changes in development | Role changes from excitatory to inhibitory as brain matures -> Cl- gradient switches |
| Dopamine synthesis/function | Synthesised from DOPA in ventral tegmental substantia nigra in brainstem -> CNS neurotransmitter/circulation hormones |
| Adrenaline synthesis | Dopamine modification -> nucleus ventrolateral to area postrema/nucleus in solitary tract dorsal region |
| NA synthesis | Adrenaline modification -> locus coeruleus |
| Serotonin synthesis/function | 5-hydroxytryptamine (derived from Trp) -> 90% produced in GI tract (regulate intestinal mvmt) -> serotonergic neurons in CNS brainstem raphe nuclei -> mood/cognition/reward/learning/memory |
| Histamine function | CNS/uterus nt -> behaviour/sleeping cycles -> degraded by histamine N-methyltransferase enzyme |
| Dopamine receptors | No ionotropic, D1/2-like metabotropic |
| NA receptors | No ionotropic, alpha1/2 and beta1/2 metabotropic |
| Serotonin receptors | 5-HT3 ionotropic, 5-HT1/2/4 metabotropic |
| Histamine receptors | Histamine gated Cl channel (CNS hypo/thalamus) ionotropic, H1 /2/3 metabotropic |
| ACh receptors | Nicotinic ionotropic, muscarinic 1-5 metabotropic |
| Phospholipase A2 receptors | Gi-alpha3 -> AA formation -> lipophilic/diffusible -> retrograde messenger (diffuses back to presynaptic terminal modulating nt release) |
| Receptor speeds | Fastest -> ionotropic, metabotropic, other transmitters, peptides/hormones, growth factors |
Created by:
vykleung
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