颈动脉注射辣椒素对脑干心血管相关核团一氧化氮合酶和Fos表达的影响

实验采用NADPH－d组化技术和Fos蛋白免疫组化技术相结合的方法,观察了颈动脉注射辣椒不时,大鼠脑干心血管相关核团内NOS和Fos蛋白的分布以及两者的共存关系。结果显示：（1）颈动脉注射辣椒不可诱发脑干中最后区（AP）、孤束核（NTS）、巨细胞旁外侧核（PGL）和蓝斑（LC）等多个部位Fos样免疫反应（FLI)神经元显著增加 中脑中央灰质（PAG）和中缝核群（RN）的FLI神经元无明显改变。（2）PGL和NTS内NO合成神经元以及PGL内双标神经元数量也明显增加,而AG和RN中NO合成神经元无明显变化,在LC和AP仅偶见或未见NO合成神经元。（3）预先应用辣椒素受体阻断剂钌红或NMDA受体阻断剂MK－801,则明显减弱辣椒素的上述效应,以上结果表明,颈动脉注射辣椒素可兴奋脑干心血管活动相关核团神经元,NO在脑干核团对辣椒素的反应中发挥间接的调制作用,辣椒素的效应由香草酸受体（辣椒素受体）介导并有谷氨酸参与。

NADPH-diaphorase activity and Fos expression in brainstem nuclei involved in cardiovascular regulation following intracarotid injection of capsaicin

The present study was undertaken to define whether intracarotid injection of capsaicin induces Fos expression associated with the activation of NOS containing neurons in brainstem nuclei by combining the immunocytochemical method for Fos with NADPH d histochemical technique for NOS. The results obtained are as follows: (1) Intracarotid injection of capsaicin caused a significant increase of Fos like immunoreactive neurons in area postrema (AP), nucleus tractus solitarius (NTS), paragigantocellularis lateralis (PGL) and locus coeruleus (LC), without influence upon the neurons of raphe nuclei (RN) and periaqueductal gray (PAG). (2) NO containing neurons in PGL and NTS and the double labeled neurons in PGL were also increased significantly following intracarotid injection of capsaicin. Small numbers of NO containing neurons were found in LC, but there was no change in the number of NO containing neurons in RN and PAG. No NADPH d histochemical activity could be found in AP. (3) The above responses to capsaicin were significantly inhibited by pretreatment with either a capsaicin receptor antagonist ruthenium red or a NMDA receptor antagonist MK 801. The above results indicate that intracarotid injection of capsaicin may activate the neurons in brainstem nuclei involved in cardiovascular regulation, and that NO only plays an indirect role in the modulation of the responses of brainstem nuclei to capsaicin. These effects of capsaicin are mediated by capsaicin receptors with involvement of glutamate.