NEURO #2.docx - NEURO #2 EXAM Introduction to...

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NEURO #2 EXAMIntroduction to Neuropharmacology-All drugs in the CNS act on specific receptors that modulate synaptic transmission and drugs are amongthe most important tools for studying all aspects of CNS physiology (from convulsions to long-termmemory).Unraveling the action of drugs with known clinical efficacy has led to some of the most fruitfulhypotheses regarding the mechanisms of disease.Tetrodotoxin: Blocks voltage gated sodium channels (source of toxin is the puffer fish).Charybdotoxin: Blocks voltage gated K channels (source scorpion).Omega-Conotoxin: Blocks voltage gated Ca channel (source pacific cone snail).Bungarotoxin: Blocks the nicotinic ACh receptor (source marine snake).Strychnine: Blocks the glycine receptor which is inhibitory (source Indian plant).-There are two types of ion channelswhich includevoltage gated(respond ONLY to membrane potentialand transmit AP from the cell body to the nerve terminalresponsible for fast AP and are usually Na orCa channels) andligand gated channels/ionotropic receptors(binding of ligand opens these channelsand these are responsible for fast synaptic transmission).-There are also two types of metabotropic receptorsalso known as G-protein coupled receptors andthese includemembrane delimited(the G protein interacts directly with the voltage gated ion channelscause the opening of K channels and the closing of calcium channels) anddiffusible secondmessengers(such as beta adrenoceptors which generate cAMPcan exert effects over considerabledistances).Metabotropic receptors predominate in the diffuse neuronal systems in the CNS.-As the AP propagate down to the axon terminal, voltage gated Calcium channels open and this causesthe fusion of synaptic vesicles with the presynaptic terminal membrane allowing for the release ofneurotransmitters.These neurotransmitters diffuse across the synaptic cleft and exert their effects onpost-synaptic G-protein coupled receptors OR ligand gated Na channels.-Excitatory post-synaptic potentials (EPSP)are due to an excitatory transmitter acting on an ionotropicreceptor causing an increase in cation permeability (results in a graded change in the size of adepolarization).Aninhibitory post-synaptic potential (IPSP)is when an inhibitory transmitter binds to achloride ionotropic channel causing a hyperpolarization (decreased membrane potential).Presynapticinhibitionis a second type of inhibition where excitatory synaptic terminals have axoaxonic synapses(reduce the amount of transmitter released from pre-synaptic neurons).-The drug targets for the pre-synaptic cellinclude the AP, transmitter synthesis, transmitter storage,metabolism, and release.Drug targets in the synapseinclude NT reuptake and degradation.Drugtargets in the post-synaptic cellinclude the ligand gated receptor, receptor induced increase/decrease inionic conductance, and retrograde signaling.NT degradation occurs in the synaptic cleft whereas NTmetabolism occurs when the NT is broken down in the pre-synaptic neuron.

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Term
Fall
Professor
Dr. Morris-Wineman
Tags
Cerebrospinal fluid, Dura mater, metabotropic receptors, amino acid NT

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