INT17459
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
[Effect of morphine on pain threshold and C-fos expression induced by substance P]. | |||||||||||||||
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Also using immunohistochemistry to identify potential intracellular mechanisms associated with alcohol-induced c-Fos expression in Edinger-Westphal, we show time-dependent increases in serine 727 phospho-signal transducer and activator of transcription 3 (Stat3) but no changes in phospho-cAMP response element-binding protein and phospho-Elk1. | |||||||||||||||
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Herein, we characterize the pharmacological and signal transduction mechanisms related to alcohol-induced c-Fos expression in Edinger-Westphal neurons. | |||||||||||||||
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Using immunohistochemistry, we show that pretreatment with gamma-aminobutyric acid (GABA)-ergic antagonists (4 mg/kg bicuculline and 45 mg/kg pentylenetetrazole) attenuates induction of c-Fos expression by alcohol (2.4 g/kg, intraperitoneal). | |||||||||||||||
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These findings suggest that alcohol-induced c-Fos expression in Edinger-Westphal results from direct interactions with GABA(A) receptors, which are modified by alpha(2A/D)-adrenoceptors and dopamine receptors. | |||||||||||||||
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The modulation of CD-induced c-fos expression exclusively in the NTS by granisetron points to a role of 5-HT(3) receptor antagonists in the modulation of vago-vagal sensomotoric reflexes rather than an influence on forebrain nuclei involved in nociception. | |||||||||||||||
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Pretreatment with granisetron significantly reduced the number of c-FLI-positive cells/section in the NTS by 40%, but had no significant effect on the CD-induced c-fos expression in other brain areas. | |||||||||||||||
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A decrease of the CD-induced c-fos expression after sensory vagal denervation by perivagal capsaicin treatment was only observed in brainstem nuclei (NTS and RVLM). | |||||||||||||||
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In all other activated brain nuclei examined, the CD-related induction of c-fos expression was diminished only after systemic neonatal capsaicin treatment. | |||||||||||||||
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Differential induction of c-fos expression in brain nuclei by noxious and non-noxious colonic distension: role of afferent C-fibers and 5-HT3 receptors. | |||||||||||||||
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Epibatidine produced a robust (2-5-fold) increase in c-Fos expression, which was not dose dependent, in all of these areas examined except the nucleus raphe magnus. | |||||||||||||||
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Vector-mediated GDNF expression blocked the nonnoxious touch-induced increase in c-fos expression in dorsal horn characteristic of the painful state. | |||||||||||||||
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Alcohol-induced c-Fos expression in the Edinger-Westphal nucleus: pharmacological and signal transduction mechanisms. | |||||||||||||||
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In addition, 10 mg/kg 2-(2,3-dihydro-2-methoxy-1,4-benzodioxin-2-yl)4,5-dihydro-1H-imidazole (RX 821002), an alpha(2A/D)-adrenoceptor antagonist, and 20 mg/kg haloperidol, a dopamine antagonist, also block alcohol-induced c-Fos expression in Edinger-Westphal neurons. | |||||||||||||||
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Studies with oligonucleotide probes for enkephalin (ENK) and dynorphin (DYN) indicated that clozapine increases c-fos expression in both ENK and DYN containing neurons in the NAc (ENK 40%, DYN 53%) and LSN (ENK 32%, DYN 59%). | |||||||||||||||
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The present results demonstrate that haloperidol and clozapine target different populations of neurons even in regions such as the NAc and LSN, where they both increase c-fos expression. | |||||||||||||||
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Haloperidol also increases c-fos expression in ENK and DYN containing neurons, albeit in a different pattern (striatum: ENK 93%, DYN 20%; nucleus accumbens: ENK 46%, DYN 36%; lateral septum: ENK 29%, DYN 18%). | |||||||||||||||
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Therefore, the sensitization of morphine-induced c-fos expression in parts of the striatum seems to correlate with the locomotor effects of repeated morphine application, whereas the observed sensitization in several limbic brain areas might reflect emotional phenomena like increased self-administration in rats or drug craving in humans. | |||||||||||||||
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In contrast, repeated dosage twice daily for 10 days and ascending from 10 to 50 mg/kg resulted in a sharply delineated morphine-induced c-fos synthesis in the dorsomedial and lateral striatum, lateral septum, medial mammillary nuclei, anterior thalamus and, in part masked by a high background due to injection stress, in the cingulate cortex. | |||||||||||||||
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CONCLUSIONS: Dibucaine and tetracaine at clinical concentrations were found to inhibit the activation of MAP kinase and the expression of c-Fos mediated by L-type Ca2+ channels in PC12 cells. | |||||||||||||||
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