Hypoxia-induced hypothermia mediated by the glutamatergic transmission in the lateral preoptic area

Hypoxia evokes a regulated decrease in the body core temperature, which response is mediated, at least in part, by noradrenaline (NA) and nitric oxide (NO) in the rostromedial preoptic area (POA) of the hypothalamus. In the accompanying paper, it was shown that glutamatergic activation of the lateral POA also evokes hypothermic responses. Here, I tested the hypothesis that the glutamatergic transmission in the lateral POA is critically involved in the neural mechanism of hypoxia-induced hypothermia. Hypoxic ventilation (10% O2–90% N2, 5 min) as well as a single microinjection of NA (50 pmol) or the NO donor sodium nitroprusside (8.4 nmol) into the rostromedial POA evoked an increase in the tail skin temperature and a decrease in the colonic temperature in urethane–chloralose-anesthetized, neuromuscularly blocked, artificially ventilated rats. All of these responses were greatly attenuated by pretreatment with multiple microinjections of kynurenic acid (10 nmol, four locations), a nonselective glutamate receptor antagonist, but not by those with saline solution, in the bilateral rostral and central parts of the lateral POA. These results suggest that the NA- and NO-sensitive structure in the rostromedial POA activated the glutamatergic transmission in the lateral POA to mediate hypoxia-induced hypothermia.

► Glutamatergic transmission was bilaterally blocked in the lateral preoptic area (POA).
► Hypothermic responses evoked by hypoxic ventilation were greatly attenuated.
► That was also the case with those elicited by noradrenaline (NA) or nitric oxide (NO).
► NA/NO in the rostromedial POA activates glutamatergic transmission in the lateral POA.
► Hypoxia-induced hypothermia is mediated by glutamate in the lateral POA.