VASOPRESSIN ANALGESIA: SPECIFICITY OF ACTION AND NON-OPIOID EFFECTS (PAIN, PEPTIDES).
Item
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Title
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VASOPRESSIN ANALGESIA: SPECIFICITY OF ACTION AND NON-OPIOID EFFECTS (PAIN, PEPTIDES).
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Identifier
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AAI8501150
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identifier
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8501150
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Creator
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KORDOWER, JEFFREY HARLAN.
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Contributor
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Richard J. Bodnar
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Date
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1984
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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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Psychology, Physiological
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Abstract
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Vasopressin (VP) has been localized in brain and spinal regions that are involved in nociceptive and stress-related behaviors. Behavioral studies have indicated that modulation of VP content, either by drug administration or with the use of a VP deficient rat strain, produce alterations in nociceptive thresholds. In addition, rats which are devoid of VP (Brattleboro strain) display an impaired analgesic response to stress. The present series of experiments aimed to determine the specificity of VP's action upon nociceptive processes, and to further assess VP's possible role in stress-induced analgesia in rats. Intracerebroventricular (icv) administration of arginine vasopressin (AVP) and desamino-D-AVP (DDAVP), in the ng range, significantly elevated pain thresholds on the tail-flick test. Oxytocin, a peptide which is synthesized in the same nuclei as VP, possesses a similar anatomical distribution as VP, and only differs from VP in two of its nine amino acids, produced seizure activity, suggesting that VP actions are not due to a general magnocellular neurosecretory effect. Central pretreatment with a VP antagonist, dPTyr(me)AVP, but not naloxone, eliminated AVP and DDAVP analgesia. Conversely, icv pretreatment with naloxone, but not dPTyr(me)AVP attenuated morphine analgesia. dPTyr(me)AVP had no effect upon basal pain thresholds. These data indicate that VP induced analgesia through interactions with its own receptors and independently of the endogenous opioids. Inhibition of ACTH, through systemic pretreatment with the synthetic glucocorticoid dexamethasone, potentiated icv VP analgesia, demonstrating that ACTH release is not necessary for the expression of VP analgesia. Lastly, icv pretreatment with dPTyr(me)AVP attenuated the analgesic response to prolonged intermittent foot shock and potentiated the analgesic response following brief continuous foot-shock. Therefore, it appears that VP plays a role in stress-induced analgesia with the direction of its effect determined by the parameters of the stress employed.
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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
