Does selective destruction of the vagal afferent inflow facilitate or reduce the development of fever?

Secondary afferent neurons in the (i) rostral commissural nucleus tractus solitarii (NTS) or (ii) caudal NTS in rats were destroyed with kainate. Lipopolysaccharide (3 mg/kg i.p.) in (i) led to a rise in colonic temperature (Tc) and random changes in the tail-flick reflex (TFR) latency. In (ii), lipopolysaccharide was not accompanied by fever, but induced a sustained hypoalgesia. In subdiaphragmatically vagotomized rats (iii) lipopolysaccharide failed to change Tc and TFR. Structural alterations in NTS and other brainstem nuclei in (iii) were electron microscopically visualized. The changes in the responses to lipopolysaccharide in the three groups may be related to degenerative events in the brainstem nuclei.