Serotonin in the Raphe Pallidus Mediates the Thermoregulatory Response to Hypoxic Stress

Evidence suggesting dysfunction in brainstem neurotransmission of serotonin (5HT) may impair proper thermoregulatory response to stress and contribute to Sudden Infant Death Syndrome (SIDS). Brainstem areas rich in 5HT, like the raphe pallidus (RaPa), mediate the thermoregulatory responses to hypoxic stress. We hypothesize that alteration in neurotransmission of the RaPa will alter the normal thermoregulatory response to hypoxic stress. Body core temperature (Tc) and selected ambient temperature (STa) were measured in conscious male Sprague‐Dawley rats using radiotelemetry. Immediately prior to hypoxic stress, the RaPa was microinjected with muscimol (GABA‐A receptor agonist) to block neurotransmission or 8‐OH‐DPAT (5HT1A receptor agonist) to alter 5HT at the RaPa. Several control groups included ACSF (control vehicle) and a sham microinjection. Tc decreased following Muscimol, ACSF, and Sham injection with hypoxia by −2.7°C, −1.1°C, and 1.1°C respectively. There was a minimal decrease in STa following Muscimol (−4.1°C), ACSF (0°C), and Sham injection (−4.9°C). 8‐OH‐DPAT injection resulted in an attenuation of the hypothermic response (−0.47°C) to hypoxia while STa slightly increased (5°C). These data suggest that the RaPa area is involved in the thermoregulatory responses to hypoxic stress. Activation of the inhibitory 5HT1A receptor attenuated the normal hypothermic response to hypoxic stress while muscimol exacerbated it. Increased understanding of the role of 5HT neurotransmission in the brain stem is vital in order to determine the etiology of SIDS and hopefully prevent its occurrence.