Cold-defense neural pathway drives stress-induced hyperthermia

      Based on in vivo physiological and neuroanatomical evidence, we have proposed a model of the central circuit mechanism for thermoregulation and fever (Nakamura, Am. J. Physiol. 301:R1207, 2011). To maintain body temperature in cold environments, the sympathetic nervous system is activated to drive thermogenesis in brown adipose tissue and cutaneous vasoconstriction. The somatic motor system also drives shivering thermogenesis. These cold-defense responses are driven by central excitatory neurotransmission from the dorsomedial hypothalamus (DMH) to sympathetic and somatic premotor neurons in the rostral medullary raphe (rMR). The level of the DMH-rMR excitatory drive is likely controlled by tonic inhibitory signaling from the thermoregulatory center, preoptic area (POA). When the POA receives cutaneous cold-sensory information through the spinal dorsal horn and the lateral parabrachial nucleus, the tonic inhibition from the POA to the DMH is attenuated, resulting in disinhibition of the DMH-rMR excitatory drive to elicit cold-defense responses. By combining optogenetics with in vivo physiology and neuroanatomy, we have recently revealed that the DMH-rMR excitatory pathway for cold defense is activated by psychological stress and can drive stress-induced brown adipose tissue thermogenesis and hyperthermia (Kataoka et al., Cell Metab. 20:346, 2014). I will introduce our recent knowledge on the central circuit mechanism for cold defense and psychological stress-induced hyperthermia.
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