Transient receptor potential vanilloid type 1 (TRPV1) activation in the Nucleus of the Solitary tract inhibits brown adipose tissue sympathetic nerve activity

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Stimulation of vagal afferent fibers or activation of neurons in the NTS (the site of vagal afferent terminals) inhibits sympathetic outflow to BAT. TRPV1 which is densely expressed in visceral vagal afferents can be directly activated by endogenous lipids to increase visceral afferent activation of neurons in the NTS. The current study investigated whether activation of TRPV1 receptors in the NTS inhibits BAT SNA and compared the level of endogenous activation of TRPV1 in rats maintained on a control chow diet or a high fat diet. In urethane/chloralose anesthetized rats maintained on a control chow diet, nanoinjection of the highly potent and selective TRPV1 receptor agonist resiniferatoxin (RTX) completely inhibited cold‐evoked BAT SNA. In rats on a control chow diet blockade of TRPV‐1 receptors in the NTS by pretreatment with the TRPV1 antagonist capsazepine (CPZ) had no effect on basal or cold‐evoked BAT SNA but prevented the RTX evoked inhibition of BAT SNA. In contrast, in rats maintained on a high fat diet for at least 8 weeks BAT SNA failed to increase during cold exposure. Nanoinjection of CPZ in the NTS reversed the HFD‐induced impairment of cooling‐evoked BAT SNA. These data demonstrate that activation of TRPV1 receptors in the NTS inhibits cold‐evoked increases in BAT SNA and suggest that in rats maintained on a high fat diet there is an elevated endogenous activation of the TRPV1 receptors in the NTS that is necessary for the high fat diet‐induced impairment of BAT activation.Support or Funding InformationSupported by American Diabetes Association Basic Science grant #1‐13‐BS‐120.