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Regulation of Acetylcholine Release From Rodent Cerebrum by Presynaptic Receptors, Methionine Enkephalin and Substance P

  • B. V. Rama Sastry
  • N. Jaiswal
  • O. S. Tayeb
Part of the Advances in Behavioral Biology book series (ABBI, volume 30)

Abstract

Acetylcholine (ACh) is released both spontaneously and upon electrical stimulation of the nerve (9). Both are dependent upon the influx of extracellular Ca++ ions. The occurrence of spontaneous release of ACh suggests that there is a steady state level of ACh in the biophase of synaptic gaps and that there may be equilibrium between the rates of influx and efflux for Ca++ ions. An ACh-amplification mechanism which suggests that the amount of ACh released by a nerve impulse is too little to effect synaptic transmission has been postulated by Koelle (8), but this ACh quickly releases further quantities of ACh to induce a postsynaptic response. A positive feedback mechanism is implicit in Koelle’s postulate because when the released amount of ACh is small, it can flood the nerve terminal to activate presynaptic cholinergic receptors, which results in the stimulation of ACh release. These presynaptic cholinergic receptors seem to be of muscarinic type (Ms) because they are activated by classical muscarinic agonists. So far, no selective agonists or antagonists have been described for these cholinergic receptors.

Keywords

Muscarinic Receptor Feedback System Phosphatidic Acid Peak Release Acetylcholine Release 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • B. V. Rama Sastry
    • 1
  • N. Jaiswal
    • 1
  • O. S. Tayeb
    • 1
  1. 1.Department of PharmacologyVanderbilt University School of MedicineNashvilleUSA

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