(C) 2008 IBRO Published by Elsevier Ltd All rights reserved “

(C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.”
“When selleck kinase inhibitor given in a warm environment MDMA (3,4-methylenedioxymethamphetamine, ecstasy) causes hyperthermia by increasing interscapular brown adipose tissue (iBAT) heat production and decreasing heat loss via cutaneous vasoconstriction. When given in a cold environment, however, MDMA causes hypothermia by an unknown mechanism. This paper addresses these mechanisms and in addition examines whether antagonists at

5-HT1A and D-2 receptors reduce the hypothermic action of MDMA. Male Sprague-Dawley rats instrumented with a Doppler probe for measuring tail blood flow, and probes for measuring core and iBAT temperatures, were placed in a temperature-control Selleck LDK378 led chamber. The chamber temperature was reduced to 10 degrees C and vehicle (0.5 ml Ringer) the 5-HT1A antagonist WAY 100635 (0.5 mg/kg), the D-2 antagonist spiperone (20 mu g/kg),

or the combination of Way 100635 and spiperone were injected s.c. Thirty minutes later the antagonists were injected again along with MDMA (10 mg/kg) or vehicle. MDMA reduced core body temperature by preventing cold-elicited iBAT thermogenesis and by transiently reversing cold-elicited cutaneous vasoconstriction. Pretreatment with WAY 100635 prevented MDMA induced increases in tail blood flow, and briefly attenuated MDMA’s effects on iBAT and core temperature. While spiperone alone failed to affect any of the parameters, the combination of spiperone and WAY 100635 decreased MDMA-mediated hypothermia by attenuating both the effects on tail blood flow and iBAT thermogenesis. MDMA’s prevention of cold-induced iBAT thermogenesis appears to have

a central origin as it rapidly reverses cold-induced increases in iBAT sympathetic nerve discharge in anesthetized PD0325901 ic50 rats. Our results demonstrate that MDMA in a cold environment reduces core body temperature by inhibiting iBAT thermogenesis and tail artery vasoconstriction and suggest that mechanisms by which this occurs include the activation of 5-HT1A and dopamine D-2 receptors. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Gastrointestinal (GI) abnormalities resulting from spinal cord injury (SCI) are challenging disorders that have not been examined experimentally using clinically relevant models. In this study, female Sprague-Dawley rats (n=5/group x 4: T10-T11 contusion, laminectomy, or naive) were fasted for 24 In before being submitted to dye recovery assays (Phenol Red solution, 1.5 ml/rat; per oral) on GI emptying/transiting at 48 h or 4 weeks postinjury (p.i.). Compared with controls, SCI significantly increased dye recovery rate (DRR, determined by spectrophotometry) in the duodenum (+84.6%) and stomach (+32.6%), but decreased it in the jejunum (-64.1% and -49.5%) and ileum (-73.6% and -70.1%) at 48 In and 4 weeks p.i.

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