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Lecture 2 Synapses Neuron-cell communication http://biolpc22.york.ac.uk/632/nervelectures.html
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Aim nto know: u mechanism of synaptic action u drugs which interfere with synaptic action u diseases of synapses
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Reading Matter nBook u Nicholls DG (1994) Proteins Transmitters and Synapses. Blackwell nPapers: u Jessell TM, Kandel ER (1993) Synaptic trans- mission - a bidirectional and self-modifiable form of cell-cell communication Cell 72S 1-30 u Whittaker, V. (1990) The contribution of drugs and toxins to understanding of cholinergic function Trends Pharm Science 11: 8-13 (in the photocopy collection)
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Revision nNeurons have channels u voltage gated u ligand gated nResting and action potentials depend on voltage gated channels nConnections between neurons usually called synapses
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Electrical connections nMembrane resistance too high for direct current flow from cell to cell gap junction
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Chemical connections nrelease chemical transmitter nrespond with receptors nadvantages u effective u excite or inhibit u variable gain ndisadvantages u slower than electrical [??]
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Examples of synaptic connections nExamples from snail neurons u Excitation u Inhibition
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Schematic diagram nneuromuscular junction
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Freeze fracture nresting nstimulated
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Quantal release nMiniature EPSP u time traces n Stimulated EPSP u overlaid traces EPSP - excitatory post-synaptic potential
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Ca ++ needed for release nCa ++ dye in presynaptic neuron n[Ca] rises at end of action potential
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Ca ++ block stops synapse npresynaptic Vm (voltage clamp) npresynaptic I Ca ++ npostsynaptic Vm
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Ca ++ block stops synapse npresynaptic EGTA blocks transmission controlEGTA
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Vesicle fusion cycling nVesicle cycling? u fusion hypothesis u kiss & run nclathrin coating fusion kiss & run
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Synaptic Toxins ntetanus & botulinum toxins u blocks transmitter release F interacts with (vesicle/membrane proteins) u produced by Clostridium bacteria
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ACh cycling ACh pumped into vesicle ACh esterase
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Summary so far ntransmitter is stored in vesicles nvesicles released calcium influx nearby ncalcium influx triggered by depolarisation from action potential
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Pharmacology of receptors nmany kinds of receptors u ACh u glutamate, glycine u serotonin, dopamine u peptides, FMRFamide nseparate pharmacologically u each receptor binds its own unique profile of drugs
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Pharmacology of receptors nNicotinic ACh receptor u agonist - nicotine, succinylcholine u antagonist - curare, bungarotoxin nMuscarinic ACh receptor u agonist - muscarine u antagonist - atropine
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Ionotropic & Metabotropic nIonotropic u receptor binding opens hole u ions flow through nmetabotropic u receptor binding activates G-protein u requires second messenger u 7 transmembrane format u phosphorylates another protein [channel]
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Second messengers nmake synapses slow ncAMP nIP3/DAG/PKC narachidonic acid = = norepinephrine
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How does 5-HT act? napply 5-HT to cell npatch elsewhere
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Effect of 5-HT n5-HT could u block a channel u reduce chance of opening u increase chance of closing u reduce current 5-HT = = serotonin
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Effect of 5-HT n5-HT closes K + channels u channel size the same u reduced chance of opening
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Summary so far ntransmitter is stored in vesicles nvesicles released calcium influx nearby ncalcium influx triggered by depolarisation from action potential nmultiple kinds of receptor u ionotropic / metabotropic u different transmitters
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Excitation and inhibition temporal summation spatial summation
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Reversal of IPSPs nInhibitory post- synaptic potentials reverse at -70 (K + ) or -50mV (Cl - )
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Pre- & Post- synaptic inhibition nPost-synaptic inhibition leads to summation of excitatory and inhibitory transmitter nPre-synaptic inhibition occurs between two axons u it prevents release of transmitter
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Transmitters & disease nmyasthenia gravis u autoimmune response to ACh receptor nParkinson’s disease u loss of dopaminergic neurons
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Confusing points to watch out for nNote the difference between u inhibition and antagonism u pre- and postsynaptic inhibition u conduction and conductance
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Summary to end ntransmitter is stored in vesicles nvesicles released calcium influx nearby ncalcium influx triggered by depolarisation from action potential nmultiple kinds of receptor u ionotropic / metabotropic F fast/slow u different transmitters nexcitatory / inhibitory
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