Site-specific modulation of morphine and swim-induced antinociception following thyrotropin-releasing hormone in the rat periaqueductal gray.
Item
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Title
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Site-specific modulation of morphine and swim-induced antinociception following thyrotropin-releasing hormone in the rat periaqueductal gray.
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Identifier
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AAI9405580
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identifier
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9405580
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Creator
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Robertson, Judith Ann.
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Contributor
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Adviser: Richard J. Bodnar
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Date
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1993
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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 | Psychology, Psychobiology
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Abstract
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Thyrotropin-releasing hormone (TRH) appears to be a potent modulator of nonopioid forms of antinociception, but produces less consistent effects upon opioid-mediated antinociception. Previous studies have examined TRH effects in ventricular, cisternal or intrathecal locations, and thus could not specify the locus of action. The mesencephalic periaqueductal gray (PAG) was chosen as a potential site for the modulatory effects of TRH because: (a) TRH-reactive fibers and receptors are localized in this area, (b) it supports TRH antinociception, and (c) it is a primary locus for supraspinal opiate analgesia. The present study examined intracerebral TRH effects upon continuous cold-water swim (CCWS) and morphine antinociception because of their clear dissociations and representations as nonopioid and opioid forms of antinociception. TRH effects upon basal nociception were also examined. Cannulated rats received intracerebral microinjections of TRH (0.1-10 ug) 20 min prior to CCWS (2{dollar}\sp\circ{dollar}C for 3.5 min) or morphine (0.1-2.5 ug) administered into the PAG. Tail-flick latencies, jump thresholds and core body temperatures were assessed in that order following the basal, CCWS or morphine conditions.;TRH microinjections into the PAG significantly increased basal tail-flick latencies and jump thresholds for up to 15 min following administration, confirming previous reports of a short-lived antinociception following supraspinal administration. Microinjections of TRH into the PAG failed to alter basal core body temperatures. TRH produced significant alterations in CCWS antinociception on the tail-flick and jump tests that varied as a function of the specific site of administration within the PAG. When TRH was microinjected into the anterior PAG, it significantly reduced CCWS antinociception on the tail-flick and jump tests in a dose-dependent fashion. In contrast, when TRH was microinjected into the posterior PAG, it significantly potentiated CCWS antinociception on the jump test. CCWS hypothermia was significantly reduced by TRH microinjections into both anterior and posterior PAG placements, suggesting a dissociation between antinociceptive and hypothermic effects.;In contrast, TRH microinjections into the both the anterior and posterior PAG significantly and dose-dependently potentiated morphine antinociception on the tail-flick and jump tests, as well as the hyperthermic effects of morphine. These results are discussed in terms of the role of the PAG in opioid and nonopioid forms of stress-induced antinociception as well as morphine antinociception, and the potential roles of TRH and the anterior PAG in a collateral inhibition model of antinociceptive responses.
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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.
