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Mechanisms of opioid adaptive behaviors.

Bryant, Camron Davis.

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Mechanisms of opioid adaptive behaviors.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Mechanisms of opioid adaptive behaviors./
作者:	Bryant, Camron Davis.
面頁冊數:	208 p.
附註:	Adviser: Christopher J. Evans.
Contained By:	Dissertation Abstracts International68-02B.
標題:	Biology, Neuroscience. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3251534

Mechanisms of opioid adaptive behaviors.
Bryant, Camron Davis.

Mechanisms of opioid adaptive behaviors. - 208 p.

Adviser: Christopher J. Evans.

Thesis (Ph.D.)--University of California, Los Angeles, 2006.

Repeated administration of opioids leads to analgesic tolerance. NMDA receptor antagonism prevents morphine analgesic tolerance, though the mechanism is unclear. It may prevent the glutamate-stimulated, calcium-mediated intracellular signaling required for changes in gene expression and the neuroplasticity that contributes to tolerance. Acute morphine administration resulted in activation of p42/44 mitogen-activated protein kinase (MAPK) in the mouse brain, a molecule involved in certain forms of synaptic plasticity, in cortical pain-related areas such as the anterior cingulate cortex (ACC). This activation did not co-localize with the mu receptor (the opioid receptor responsible for analgesia and reward) and was NMDA receptor-dependent, suggesting that MAPK-induced synaptic plasticity occurs in cells downstream of mu receptor activation. The non-competitive NMDA receptor antagonist MK-801 attenuated morphine analgesic tolerance in the hot plate assay, yet surprisingly, facilitated it in the tail withdrawal assay in male, but not female mice. Ovariectomy had no effect, suggesting the contribution of organizational effects of gonadal steroids.Subjects--Topical Terms:

1017680
Biology, Neuroscience.

Mechanisms of opioid adaptive behaviors.
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100 1 $a Bryant, Camron Davis. $3 1296508
245 1 0 $a Mechanisms of opioid adaptive behaviors.
300 $a 208 p.
500 $a Adviser: Christopher J. Evans.
500 $a Source: Dissertation Abstracts International, Volume: 68-02, Section: B, page: 0791.
502 $a Thesis (Ph.D.)--University of California, Los Angeles, 2006.
520 $a Repeated administration of opioids leads to analgesic tolerance. NMDA receptor antagonism prevents morphine analgesic tolerance, though the mechanism is unclear. It may prevent the glutamate-stimulated, calcium-mediated intracellular signaling required for changes in gene expression and the neuroplasticity that contributes to tolerance. Acute morphine administration resulted in activation of p42/44 mitogen-activated protein kinase (MAPK) in the mouse brain, a molecule involved in certain forms of synaptic plasticity, in cortical pain-related areas such as the anterior cingulate cortex (ACC). This activation did not co-localize with the mu receptor (the opioid receptor responsible for analgesia and reward) and was NMDA receptor-dependent, suggesting that MAPK-induced synaptic plasticity occurs in cells downstream of mu receptor activation. The non-competitive NMDA receptor antagonist MK-801 attenuated morphine analgesic tolerance in the hot plate assay, yet surprisingly, facilitated it in the tail withdrawal assay in male, but not female mice. Ovariectomy had no effect, suggesting the contribution of organizational effects of gonadal steroids.
520 $a Genetic differences exist in the degree of morphine analgesic tolerance with the 129S6 and 129P3 mouse strains reportedly lacking tolerance. In contrast, we found substantial tolerance in both strains. Analysis of previous studies indicated that rotarod performance frequently correlated with tolerance susceptibility across several inbred mouse strains. This suggests a common underlying genetic mediation of these two seemingly unrelated behaviors. The working hypothesis is that the 129 substrains exhibit a weakened nociceptive response during the tolerant state, perhaps via the inherent abnormal myelination of the ventral root in this strain. One question is whether strain differences in the degree of morphine tolerance can be explained by strain differences in the intensity of the nociceptive response during the morphine-tolerant state.
520 $a Last, one injection of fentanyl in a novel environment elicited several conditional opioid-like behaviors in response to a subsequent placebo injection including conditional locomotion, pattern of locomotion, Straub tail, analgesia, and place preference. Conditional place preference, but not locomotion, was dependent on the endogenous opioid system, indicating that the two behaviors are independent. Future experiments involving the selective disruption of opioid reward may reveal its contribution to the establishment of the placebo effect.
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791 $a Ph.D.
792 $a 2006
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