BIOL 361 : Bio361-neurotransmitter release

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Ap reaches the mem of the presynaptic axon terminal of the nmlar junction- 2. resulting deplzatn ->vg ca2+channels opening on the cell mem of the axon terminal 3. both []+electrical gradient(eqlm. pot-ca=130mv, rmp= +co(coenzyme)a**signaling btw a ligand(ex. neutrsmter+receptor)must be terminated in order to be effective-acetylcholinesterase-speci c enzyme in the synapse,removes ach from its receptor+breaking the ach down into choline. >opening a pore in the middle of the receptor->allow ions to cross the mem->rapid excitatory postsynaptic potent);has relatively nonselective channel(permeable to. >reduce signal intensity@postsynaptic muscle cell->reduce strength of muscle contraction->muscle weakness)-drug= acetylcholinesterase inhibitors(nerve gas sarin)-reduce rate of removal of ach from receptor(inhibit degradation of. Ach)=increase [ach] in the synapse= compensate for the decreased#of ach receptors =reduce symptoms of muscle weakness+fatigue(high dose= increase the [ach] in the synapse=overexcitation of the muscle->twitching, muscle fatigue, paralysis in resp. muscle->death)! +aspartate+glycine(used for protein synthesis),gama-aminobutyric(gaba; derivative of glutamate);act as chem. msger+obtain from fd,once synthesized-get packaged into vesicles until released by exocytosis-neuropeptides/neuroactive peptides/peptide neutrsmters-short chains of aa, synthesized in the.

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