Functional relationship between the amygdala and periaqueductal gray in the processes of pain and analgesia.
Item
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Title
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Functional relationship between the amygdala and periaqueductal gray in the processes of pain and analgesia.
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Identifier
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AAI9820570
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identifier
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9820570
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Creator
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Pavlovic, Zoran M.
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Contributor
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Mentor: Richard J. Bodnar
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Date
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1998
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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 | Psychology, Physiological
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Abstract
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The amygdala is a temporal lobe structure that is involved in the processes of fear and anxiety, conditional emotional responses, learning and memory, aggression, stress, and analgesia. It has extensive two-way projections with brainstem structures, such as the periaqueductal gray (PAG), which is part of endogenous antinociceptive circuitry.;Microinjections of either morphine and beta-endorphin in the amygdala significantly increased tail-flick latencies and jump thresholds. The increases were far more pronounced on the jump test than on the tail-flick test. Placements dorsal and medial to the amygdala were ineffective PAG pretreatment with either general (naltrexone), delta{dollar}\sb2{dollar} (NTII) and to a lesser degree mu (BFNA) opioid antagonists significantly reduced both morphine and beta-endorphin analgesia elicited from the amygdala. These data indicate that PAG delta{dollar}\sb2{dollar} and to a lesser degree mu opioid receptors are necessary for the full expression of morphine and beta-endorphin analgesia elicited from the amygdala.;This dissertation then characterized functional analgesic interactions between the amygdala and the PAG by examining multiplicative interactions for sub-effective doses of morphine and beta-endorphin simultaneously applied to these two structures. Co-administration of subthreshold doses of either morphine or beta-endorphin into both the amygdala and the PAG, as well as when beta-endorphin was microinjected in the amygdala and morphine in the PAG, produced a potent synergistic interaction. However, co-administration of morphine in the amygdala and beta-endorphin in the PAG failed to produce an interactive effect. This result argues for multiple modulatory mechanisms mediating beta-endorphin analgesia in the PAG, which is not the same as for morphine. Co-administration of subeffective doses of morphine and beta-endorphin into either the amygdala alone or the PAG alone failed to produce an interaction, thus indicating the importance of regional opioid activation.;Finally, microinjections of the kappa1 opioid agonist, U58488H in the amygdala elicited test-specific analgesia on the jump test and not the tail-flick test. Like morphine and beta-endorphin analgesia, U50488H-induced analgesia elicited from the amygdala was blocked by PAG preatreatment with general and mu, but not delta antagonists, indicating mediation by mu opioid synapses in the PAG.;These data collectively implicate the amygdala as a part of endogenous antinociceptive circuitry and points towards its elaborate functional analgesic interactions with the PAG. These data also integrate opioid analgesic systems in the amygdala with the structure's previously known roles in fear and stress.
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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.
