batman
Forum Newbie
Topics: 9
Posts: 10
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How would a change in the rate of NTS (Neurotransmitter Substance?) inactivation alter the ability of an autonomic pathway to control the function of an effector cell?
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| Zat
Forum Senior
Topics: 2
Posts: 26
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Hi batman, i wonder where you got that question from, it's full of unusual terminology.
I would be able to reformat that question in other words: for example....
How would a change in the rate of AcetylCholine inactivation affect the autonomic system neural outflow?
Also,....
Neurotransmitter substances are inactivated in one of the following ways:
1- Enzymatic destruction (Acetytransferase in ACh)
2- Reuptake by the presynaptic membrane (NE in adrenergic transmission)
3- Diffusion away from the site of action
Therefore, how would a change in any of these three mechanisms change the amount of sympathetic/parasympathetic outflow?
This is the basis of many pharmacological agents, such as, Acetylcholine esterase inhibitors (myesthenia gravis treatment) , MAO inhibitors (antidepressants), SSRI (antidepressants), alpha 2 centrally acting agonists (anti hypertensive), and many more.
Bottom line:
increasing rate of NTS inactivation----> decrease availibity of NTS at postsynaptic receptors -----> decrease control of ANS on effector cell
and vice versa.....
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| mildus
Forum Guru
Topics: 19
Posts: 614
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Nice post Zat
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