It has been reported that systemic injection of arginine vasopressin (AVP) induces a drop in body core temperature (T_c), but little is known about the mechanisms involved. Because glutamate is an important excitatory neurotransmitter involved in a number of thermoregulatory actions, in the present study, we tested the hypothesis that glutamate plays a role in systemic AVP-induced hypothermia. Wistar rats were pretreated intracerebroventricularly (icv) with kynurenic acid, an antagonist of L-glutamate ionotropic receptors, -methyl-(4-carboxyphenyl)glycine (MCPG), an antagonist of L-glutamate metabotropic receptors, or saline 15 min before intravenous injection of AVP (2 µg/kg) or saline. T_c, brown adipose tissue (BAT) temperature, blood pressure, heart rate, and tail skin temperature were measured continuously. Administration of saline icv followed by intravenous AVP caused a significant drop in T_c brought about by a reduction in BAT thermogenesis and an increase in heat loss through the tail. MCPG treatment (icv) did not affect the fall in T_c induced by AVP. Treatment with kynurenic acid (icv) abolished AVP-induced hypothermia but did not affect the AVP-evoked rise in blood pressure or drop in heart rate and BAT temperature. Heat loss through the tail was significantly reduced in animals injected with AVP and pretrated with kynurenic acid. These data indicate that ionotropic receptors of L-glutamate in the central nervous system participate in peripheral AVP-induced hypothermia by affecting heat loss through the tail.