Unformatted text preview: onic transmission of both subdivision do involve acetylcholine. acetylcholine do act on nico-recep to cause ESP, but it
cause act on muscarinic to generate slow EPSP. the slow epsp is due to closing of potassium channel (depolarize?>???). slow IPSP is due to acetyl bind to musc,
cause increase potassium perme, cause hyperpo since Ek is more negative than membrane potential.
-peptide work with ACh. synapse is not just relay center. on para post-gang side neuro is acetylcho, bind to muscine. different parasymp neruon release varying
amount of VIP (vasoactive intestinal peptide). VIP have strong vasodilating effect (cause arteriole and smooth muscle relaxation, increase blood flow). VIP causes
variety of effects in other target tissue. in the intestine or GI tract, ACE+VIP ARE synergic (salivary gland, parasymp cause saliva secretion, help through
vasodilation). VIP stimulate motilibity, digestion, movement.
-on symp, main neurotr release from postg is noerp act on different adnergic receptors. different target cells express different ratios of adnergic receptors, have
different effects through different second messengers. most postgang release no, except at postga for sweat gland which release acetylcholine. act on nicotinic
-there are also cosubstance: atp bind to atp receptor or purine receptor. ATP is very unstable, rapidly degraded. degraded form bind to p1 or p2. have synergistic
effect. the ones below the line modulate the effects on top.
-target for specific drug. to reduce blood pressure by slowing down heart rate w.o other effects then it's useful to know that release noepri acting through beta 1 drug Preganglionic Postganglionic ACh + Peptides ACh Target Cells Muscarinic AChRs Parasymp.
+/- VIP VIP-R Norepi α1, α2, β1, β2, β3 ARs or ACh nAChRs + ATP
+ peptides P1, P2 Rs
various Rs nAChRs (fast EPSP)
mAChRs (slow EPSP or IPSP) Symp.
ACh + Peptides...
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- Spring '09
- heart rate, target organ