Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pregnancy is associated with an antinociception that is multifactorial and results from spinal (kappa/delta) opioid antinociceptive pathways as well as peripheral processes (ovarian sex steroids, uterine afferent neurotransmission). The present results provide the first indication that the full manifestation of pregnancy-induced analgesia also requires a supraspinal component. The analgesia of gestation or its hormonal simulation (via estrogen and progesterone administration; HSP) is substantially attenuated (>/=60%) following blockade of spinal alpha(2) (but not alpha(1)) adrenergic receptors. HSP antinociception is also attenuated by transection of the hypogastric nerve, the magnitude of which is indistinguishable from that produced by spinal alpha(2) receptor blockade. Additionally, hypogastric neurectomy abolishes the component of the antinociception associated with HSP that is mediated by spinal alpha(2) receptors. This suggests that the augmented spinal noradrenergic activity during HSP is not due to activation at the terminal of noradrenergic spinal projection neurons but requires supraspinal activity. It is suggested that enhanced spinal noradrenergic activity amplifies ongoing spinal kappa/delta antinociception as has been observed following the concomitant intrathecal application of alpha(2) and opioid agonists. The current observations underscore the importance of visceral afferent activity as well as its modulation by a female-specific hormonal milieu to the efficacy of endogenous spinal opioid antinociception.
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PMID:Gestational and ovarian sex steroid antinociception: relevance of uterine afferent and spinal alpha(2)-noradrenergic activity. 1053 9

Opiates are the most effective drugs for pain relief. However, the repeated use of opiates induces tolerance to their analgesic effects. It has been shown that this morphine-induced tolerance is associated with apoptosis in the central nervous system. The aim of this study is to evaluate the effects of intracerebroventricular (i.c.v.) administration of riluzole, an anti-glutamatergic drug, on morphine-induced apoptosis in the lumbar region of the rat spinal cord. Animals were given daily injections of morphine and vehicle, morphine and riluzole, or riluzole alone. Nociception was assessed using a hot plate apparatus, and apoptosis was assessed using the in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method. The levels of anti-apoptotic factors Bcl-2 and HSP 70 and the pro-apoptotic agent caspase-3 were evaluated using immunoblotting. The glutamate concentration in the lumbar spinal cord was measured with high performance liquid chromatography (HPLC). The results indicate that the i.c.v. administration of riluzole attenuated morphine tolerance and reduced the number of TUNEL positive cells. Immunoblotting revealed that the levels of the selected anti-apoptotic agents were greater in the treatment groups compared to the controls. Furthermore, the results demonstrated that the administration of riluzole can attenuate the morphine-induced elevation of glutamate in the lumbar spinal cord. In conclusion, i.c.v. administration of riluzole attenuated morphine-induced tolerance to analgesia and apoptosis in addition to preventing the morphine-induced increase of glutamate in the lumbar spinal cord of rats.
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PMID:Intracerebroventricular administration of riluzole prevents morphine-induced apoptosis in the lumbar region of the rat spinal cord. 2088 6