CHOLINERGIC INVOLVEMENT IN PAIN INHIBITION (STRESS INDUCED ANALGESIA, ACETYLCHOLINE, SCOPOLAMINE).
Item
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Title
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CHOLINERGIC INVOLVEMENT IN PAIN INHIBITION (STRESS INDUCED ANALGESIA, ACETYLCHOLINE, SCOPOLAMINE).
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Identifier
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AAI8629691
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identifier
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8629691
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Creator
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SPERBER FREEBERN, ELLEN.
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Contributor
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Richard J. Bodnar
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Date
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1986
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Language
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English
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Publisher
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City University of New York.
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Subject
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Biology, Neuroscience
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Abstract
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Acetylcholine and its receptor agonists increase pain thresholds and may be important in the meditation of opioid and non-opioid forms of pain inhibition. The present study assessed the effect of muscarinic receptor antagonists, scopolamine (0.001-10.0 mg/kg) and methylscopolamine (1.0-10.0 mg/kg) upon analgesia induced by cold-water swims (CWS), 2-deoxy-D-glucose (2DG) glucoprivation, forepaw (FPS) and hindpaw (HPS) footshock, pilocarpine, D-ala-D-leu-enkephalin (DADL), beta-endorphin (BEND) or morphine. Scopolamine and methylscopolamine significantly reduced CWS analgesia on the jump test 30 min after the swim and eliminated this effect 60 min following the swim. In contrast, both muscarinic receptor agonists potentiated CWS analgesia on the tail-flick test and increased CWS hypothermia effects and these were correlated. Scopolamine and methylscopolamine increased the duration of 2DS analgesia, particularly on the jump-test. However, both muscarinic receptor antagonists reduced 2DG hyperphagia in a dose-dependent manner. This effect was correlated with the ability of scopolamine and methylscopolamine to reduce basal food intake. In contrast to their mediation of the neurohormonal analgesic responses of CWS and 2DG, neither scopolamine nor methylscopolamine altered neurally mediated FPS of HPS analgesia. Scopolamine, but not methylscopolamine, eliminated pilocarpine analgesia on the jump test and tail-flick test indicating differences in cholinergic mediation of CWS analgesia relative to this muscarinic receptor agonist. Scopolamine and methylscopolamine effects upon analgesic and other stress responses could not be attributed to shifts in baseline jump thresholds, tail-flick latencies or core body temperature changes. Despite the postulated synergy between cholinergic and opiate agonists, scopolamine potentiated DADL and morphine, but not BEND analgesia on the jump test. These results indicate that the cholinergic system mediates pain inhibition independently of the endogenous opiate system. The different patterns of reductions in CWS and pilocarpine analgesia by muscarinic antagonists suggest peripheral and central cholinergic influences. That some analgesic responses are reduced while others are potentiated by muscarinic receptor antagonism provides further evidence for heterogeneity in pain inhibition and possible collateral inhibition exerted between systems.
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Type
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dissertation
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Source
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PQT Legacy CUNY.xlsx
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degree
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Ph.D.
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Program
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Psychology
