Thermoregulatory responses elicited by microinjection of l-glutamate and its interaction with thermogenic effects of GABA and prostaglandin E2 in the preoptic area

The aim of the present study was to investigate the thermoregulatory effects of neuronal activation with sodium l-glutamate (glutamate) in the preoptic area (POA) of the hypothalamus and to examine its possible interaction with the thermogenic effects of GABA and prostaglandin E2 (PGE2). Unilateral microinjection of glutamate (5 nmol) into the lateral POA or its vicinity elicited a prompt increase in tail skin temperature and simultaneous decreases in the O2 consumption rate (VO2), heart rate, and colonic temperature in urethane–chloralose-anesthetized rats. A central subpopulation of these sites at around the level of bregma was also responsive to the thermogenic and tachycardic effects of GABA (30 nmol). Although the microinjection of GABA into nearby sites elicited no direct effect, it greatly attenuated the hypothermic effects of glutamate subsequently administered to the same site. These results suggest that activation of the lateral POA elicited heat-loss responses and that its central part provided a tonic inhibitory drive toward heat production and tail vasoconstriction. On the other hand, the microinjection of glutamate elicited initial small decreases and subsequent large increases in VO2 and heart rate in the rostromedial POA. However, no thermoregulatory response was elicited by the microinjection of glutamate at sites where the microinjection of PGE2 (35 fmol) elicited thermogenic, tachycardic and hyperthermic responses. These results may suggest that the rostromedial POA contained two glutamate-responsive cell groups that had opposite influences on thermoregulation and that the locus that was highly sensitive to the thermogenic effect of PGE2 was unreactive to glutamate. Collectively, activation of neurons in the lateral POA and rostromedial POA evoked distinct thermoregulatory responses.

► Activation of the lateral preoptic area (POA) elicits heat loss responses.
► Inhibition of its central part evokes heat production.
► Activation of the rostromedial POA evokes biphasic changes in thermogenesis.
► The locus that is highly sensitive to prostaglandin E2 is unreactive to glutamate.