Effect of cervical vagotomy on sympathetic nerve responses to peripheral interleukin-1beta.

Although the vagus nerve is an important neural pathway mediating immune-to-brain communication, the role of the vagus in mediating sympathetic nerve discharge (SND) responses to peripheral cytokines is not well established. In the present study we determined renal, interscapular brown adipose tissue (IBAT), splenic, and lumbar SND responses before and for 60 min after the intravenous administration of interleukin-1beta (IL-1beta, 100 ng) in chloralose-anesthetized, sham-vagotomized and cervical-vagotomized (bilateral) rats. In sham-vagotomized rats, IL-1beta administration increased (P<0.05) splenic and lumbar SND while renal and IBAT SND remained unchanged from control levels. Renal, splenic, and lumbar SND were increased (P<0.05) whereas IBAT SND remained unchanged from control after IL-1beta in vagotomized rats. Renal, splenic, and lumbar SND responses were significantly higher after IL-1beta in vagotomized compared with sham-vagotomized rats. These results demonstrate that regionally-selective SND (renal, splenic, and lumbar) responses to IL-1beta can occur in the absence of the vagus nerve and suggest that the vagus nerve provides a tonic inhibition to the discharges in these nerves in response to peripheral IL-1beta.

Effects of midbrain and spinal cord transections on sympathetic nerve responses to heating.

In the present study, we investigated the contributions of forebrain, brain stem, and spinal neural circuits to heating-induced sympathetic nerve discharge (SND) responses in chloralose-anesthetized rats. Frequency characteristics of renal and splenic SND bursts and the level of activity in these nerves were determined in midbrain-transected (superior colliculus), spinal cord-transected [first cervical vertebra (C1)], and sham-transected (midbrain and spinal cord) rats during progressive increases in colonic temperature (T(c)) from 38 to 41.6-41.7 degrees C. The following observations were made. 1) Significant increases in renal and splenic SND were observed during hyperthermia in midbrain-transected, sham midbrain-transected, C1-transected, and sham C1-transected rats. 2) Heating changed the discharge pattern of renal and splenic SND bursts and was associated with prominent coupling between renal-splenic discharge bursts in midbrain-transected, sham midbrain-transected, and sham C1-transected rats. 3) The pattern of renal and splenic SND bursts remained unchanged from posttransection recovery levels during heating in C1-transected rats. We conclude that an intact forebrain is not required for the full expression of SND responses to increased T(c) and that spinal neural systems, in the absence of supraspinal circuits, are unable to markedly alter the frequency characteristics of SND in response to acute heat stress.

Cold stress alters characteristics of sympathetic nerve discharge bursts.

Frequency-domain analyses were used to determine the effect of cold stress on the relationships between the discharge bursts of sympathetic nerve pairs, sympathetic and aortic depressor nerve pairs, and sympathetic and phrenic nerve pairs in chloralose-anesthetized, baroreceptor-innervated rats. Sympathetic nerve discharge (SND) was recorded from the renal, lumbar, splanchnic, and adrenal nerves during decreases in core body temperature from 38 to 30 degrees C. The following observations were made. 1) Hypothermia produced nonuniform changes in the level of activity in regionally selective sympathetic nerves. Specifically, cold stress increased lumbar and decreased renal SND but did not significantly change the level of activity in splanchnic and adrenal nerves. 2) The cardiac-related pattern of renal, lumbar, and splanchnic SND bursts was transformed to a low-frequency (0-2 Hz) pattern during cooling, despite the presence of pulse-synchronous activity in arterial baroreceptor afferents. 3) Peak coherence values relating the discharges between sympathetic nerve pairs decreased at the cardiac frequency but were unchanged at low frequencies (0-2 Hz), indicating that the sources of low-frequency SND bursts remain prominently coupled during progressive reductions in core body temperature. 4) Coherence of discharge bursts in phrenic and renal sympathetic nerve pairs in the 0- to 2-Hz frequency band increased during mild hypothermia (36 degrees C) but decreased during deep hypothermia (30 degrees C). We conclude that hypothermia profoundly alters the organization of neural circuits involved in regulation of sympathetic nerve outflow to selected regional circulations.