CAJ | 학술논문

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素时, 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) 颈动脉注射辣椒素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, 而中脑中央灰质(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PAG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。
실험채용NADPH-d 조화기술화Fos 단백면역조화기술상결합적방법, 관찰료경동맥주사랄초소시, 대서뇌간심혈관상관핵단내NOS화Fos단백적분포이급량자적공존관계。결과현시: (1) 경동맥주사랄초소가유발뇌간중최후구(AP)、고속핵(NTS)、거세포방외측핵(PGL)화람반(LC)등다개부위Fos양면역반응(FLI)신경원현저증가, 이중뇌중앙회질(PAG)화중봉핵군(RN)적FLI신경원무명현개변。(2) PGL화NTS 내NO합성신경원이급PGL내쌍표신경원수량야명현증가, 이PAG화RN중 NO합성신경원무명현변화, 재LC화AP부우견혹미견NO합성신경원。(3) 예선응용랄초소수체조단제조홍혹NMDA수체조단제MK-801, 칙명현감약랄초소적상술효응。이상결과표명, 경동맥주사랄초소가흥강뇌간심혈관활동상관핵단신경원, NO재뇌간핵단대랄초소적반응중발휘간접적조제작용, 랄초소적효응유향초산수체(랄초소수체)개도병유곡안산삼여。
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.