Changes in the phosphorylation of cAMP response element binding protein in the rat nucleus accumbens after acute and chronic ethanol administration / 生理学报

To define the molecular basis of ethanol dependence, changes in the phosphorylation of cAMP response element binding protein (CREB) in the nucleus accumbens of rats after acute and chronic ethanol administration were detected using immunohistochemistry. The results demonstrate that the expression of phospho-CREB (p-CREB) protein in the rat nucleus accumbens significantly increased after 15 min of acute ethanol exposure, reaching a peak at 30 min after ethanol administration. The increment remained after 1 or 6 h of ethanol exposure compared to the control rats. In contrast, chronic intake of ethanol solution obviously decreased the expression of p-CREB protein compared to the control rats. The decrement remained 24 h or 72 h after ethanol withdrawal, and returned to the control levels after 7 d of ethanol withdrawal. The results suggest that an acute ethanol administration led to an increase in the phosphorylation of CREB in the nucleus accumbens, but chronic ethanol administration produced a decrement, which is possibly one of the molecular mechanisms of alcohol dependence.

The effects of neuropeptides on the regulations of gastric mucosal blood flow in central nervous system and periphery in rats / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effects of calcitonin gene-related peptide (CGRP), gastrin 17 (G17), bombesin (Bom), met-enkephalin (Met-enk), neuropeptide Y (NPY) and somatostatin (SS) on GMBF and the role of endogenous NO in increased GMBF induced by neuropeptides in rats.</p><p><b>METHODS</b>By hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF) and arterial infusion close to stomach or intracerebroventricular (icv) to microinject neuropeptides.</p><p><b>RESULTS</b>(1) Arterial infusions of CGRP and G17 (5, 50 and 100 pmol x min(-1)) increased GMBF significantly in dose-dependent manners. CGRP had more effective effect on increasing GMBF than that of G17. Intravenous pretreatment of L-nitro-L-arginine methyl ester (L-NAME) to inhibit the synthesis of endogenous NO could abolish completely or partially the increases in GMBF response to CGRP or G17 respectively. (2) Arterial infusions of Bom and Met-enk (50 and 100 pmol x min(-1)) increased GMBF significantly. The increases in GMBF induced by Bom or Met-enk were abolished completely or partially by pretreatment of L-NAME respectively. (3) Arterial infusion of NPY (5, 50 and 100 pmol x min(-1)) led to reduction of GMBF significantly in a dose-dependent manner. SS (50 and 100 pmol x min(-1)) also reduced GMBF significantly. (4) icv microinjection of CGRP (10 microg) and G17 (10 Microg) increased GMBF significantly. The increases in GMBF induced by icv microinjection of CGRP or G17 were blocked completely or partially respectively by pretreatments with L-NAME. (5) icv microinjection of NPY (10 microg) decreased GMBF significantly.</p><p><b>CONCLUSION</b>Neuropeptides play important roles in the regulation of GMBF in rats and NO is involved in the increase of GMBF induced by some neuropeptides.</p>