Abstract
Stress-induced hyperthermia is a well-known component of the response to stress in mammals. Neurons in the dorsomedial hypothalamus (DMH) play an important role in thermoregulatory adjustments, but the role of the DMH in stress-induced hyperthermia has yet to be examined. We have previously shown that microinjection of non-selective ionotropic glutamate receptor (iGR) antagonists into the DMH suppresses stress-induced tachycardia. Here we tested the hypothesis that iGRs in the DMH mediate the increase in core body temperature seen in experimental stress in conscious rats. Male SD rats were instrumented with bilateral guide cannulas targeting the DMH and intraperitoneal telemetric transmitters for monitoring core body temperature. Cage switch evoked significant increases in core body temperature that were abolished by prior microinjection of the non-selective iGR receptor antagonist, kynurenic acid (10nmol/side), into the DMH. Similar microinjection of a cocktail of an N-methyl-D-aspartate (NMDA) iGR antagonist, 2-amino-phosphonopentanoic acid, (APV; 200pmol/side) and a non-NMDA iGR antagonist, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)-quinoxaline-2,3-dione, (NBQX; 100pmol/side) also abolished these increases. These findings suggest that stress-induced hyperthermia may be mediated by iGRs in the DMH. (Supported by USPHS Grants MH 65697 and NS 19883, and F31 NS052929 to MYM)
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