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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© 2015 Published by Elsevier Inc.