Role of vagal afferent innervation in feeding and brain Fos expression produced by metabolic inhibitors.

Hepatic vagal afferent fibers have been implicated in the feeding responses initiated by administration of 2,5-anhydro-D-mannitol (2,5-AM; an inhibitor of hepatic metabolism) and methyl palmoxirate (MP; an inhibitor of fat metabolism). 2,5-AM and MP also increase brain Fos expression, an indicator of neural activity, which suggests that Fos expression can reveal the central neural pathways involved in the stimulation of feeding by these agents. To more closely test the hypothesis that brain Fos expression is related to the effects of 2,5-AM and MP on feeding, the vagus was lesioned by application of capsaicin, which destroys afferent fibers, directly to the cervical vagi. Perivagal capsaicin treatment blocked 2,5-AM-induced eating and attenuated MP-induced eating. Although perivagal capsaicin treatment attenuated MP-induced Fos expression, capsaicin treatment did not affect brain Fos expression produced by 2,5-AM. It is concluded that (1) brain Fos expression is not always related to the effects of 2,5-AM on feeding, (2) capsaicin-sensitive hepatic vagal afferent fibers carry the signal that stimulates feeding following 2,5-AM treatment, and (3) MP-induced feeding and brain Fos expression is mediated in part by capsaicin-sensitive fibers.