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Stereospecific enhancement of evoked release of brain acetylcholine by narcotic antagonists
Author(s) -
Jhamandas Khem,
Sutak Maaja
Publication year - 1983
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1983.tb09408.x
Subject(s) - acetylcholine , (+) naloxone , endocrinology , medicine , naltrexone , hypophysectomy , enkephalin , stimulation , chemistry , inhibitory postsynaptic potential , opioid peptide , endogenous opioid , pharmacology , opioid , receptor , hormone
1 Electrical stimulation of nerves in the forepaw of anaesthetized rats caused an increase in the release of acetylcholine (ACh) from the cerebral cortex in vivo. Actions of naloxone (Nal) enantiomers and naltrexone (Ntx) were tested on this release in normal animals and those lacking pituitary gland for 3 weeks. 2 In normal animals systemic administration of (−)‐Nal or Ntx, but not (+)‐Nal caused a significant increase in the evoked release of ACh. Spinally administered (−)‐Nal did not produce this effect. Cortical application of (−)‐Nal produced a smaller increase in the evoked release of ACh. 3 In hypophysectomized rats the stimulatory action of (−)‐Nal or Ntx on ACh release was significantly reduced. The ability of (−)‐Nal to reverse inhibitory action of morphine or the enkephalin (FK 33,824) was not affected by hypophysectomy. 4 It is suggested that (−)‐Nal and Ntx increase the stimulated release of cortical ACh by blocking the inhibitory action of an endogenous opioid at a subcortical site. An intact pituitary appears essential for a full expression of the Nal effect on evoked ACh release.