大鼠臂旁外侧核化学毁损对脂多糖致热反应的影响.

Objective：To investigate the effect of lateral parabrachial (LPB)chemical lesion on the fever induced by lipopolysaccharide (LPS), and to clarify whether LPB was involved in the fever induced by LPS. Methods：Twelve adult male SD rats were randomly divided into control group and LPB-lesion group (n=6). The rats in LPB-lesion group were bilaterally injected with ibotenic acid into LPB by nuclear injection to induce chemical lession, and the rats in control group were injected with the equal amount of saline into LPB. The rats were survived for at least 1 week and then were implantated with telemetry transmitter for monitoring the body core temperature (Tcore) in the abdominal cavity. The Tcore and activities of the rats in two groups at different time points after intraperitoneal injection of normal saline or LPS were monitored by radiotelemetry, and the distributions of NeuN and Nissl bodies in LPB of the rats in two groups were detected by immunofluorescence staining and Nissl staining. Results: The rats in control group were induced the typically biphasic fever after intraperitoneal injection of LPS (100 μg·kg－1), and the Tcore started to rise 1.5 h after intraperitoneal injection of LPS, firstly reached its peak at 2. 5 h (the first phase), started to rise again at 3. 5 h and reached its peak again at 5. 5 h (the second phase)after injection of LPS; the rats in LPB-lesion group also had fever reaction after intraperitoneal injection of LPS. At 5.5 h, the Tcore was significantly higher than the basic Tcore (P<0. 05)；compared with control group, the fever reaction of the rats in LPB-lesion group was significantly weakened, and the increasing of Tcore at 2.5 and 5. 5 h after intraperitoneal injection of LPS was lower than that in control group (P<0. 05). After intraperitoneal injection of normal saline or LPS, the activities of the rats in control group and LPB-lesion group were increased temporarily compared with those before injection, but there were no significant differences between two groups (P>0. 05). A large number of NeuN immunopositive neurons were distributed in LPB of the rats in control group, with large number of Nissl bodies and the shape was big, and the morphology of the cells was complete and the margin was clear；in LPB-lesion group, there were almost no NeuN immunoreactive neurons in the LPB lesion area at the rostral, middle, and caudal levels in the rostrocaudal directions, the neuronal soma was missing, and the Nissl bodies were largely disappeared. Conclusion：LPB chemical lession model partially eliminate the LPS-induced fever, indicating that LPB plays a role in the LPS-induced fever. [ABSTRACT FROM AUTHOR]