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The dependence of thermogenesis on the availability of metabolic substrates suggests
that vagally-transmitted, metabolic signals from the viscera could influence the central
neural systems driving the BAT and shivering thermogenesis that normally contributes
to the cold-defensive maintenance of core body temperature and to the elevated temperature
during fever. We tested this hypothesis by electrically stimulating viscerosensory
afferents in the proximal end of the sectioned cervical vagus nerve in Inactin-anesthetized,
ventilated rats while recording BAT sympathetic nerve activity (SNA) and nucal EMG.
Continuous VNS at 10Hz produced a complete inhibition of cold-evoked BAT SNA and shivering
EMG activity. Similar inhibitions of BAT and shivering thermogenesis follow activation
of neurons in the nucleus of the solitary tract (NTS) or those in the caudal ventrolateral
medulla (cVLM). These data support the existence of populations of vagal afferents
whose stimulation can inhibit the generation of BAT sympathetic and shivering EMG
activities, perhaps via activation of thermogenesis-inhibiting neurons in the NTS
and the cVLM (see Am. J. Physiol. Regul. Integr. Comp. Physiol., 299:R277-R290, 2010).
Supported by NIH grants NS040987 and NS091066.
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