目的探讨运动刺激前庭感受器后,下丘脑室旁核(Pa)神经元的反应,及Pa在前庭刺激引发机体自主反应中的作用和有关神经机制。方法将10只成年雄性SD大鼠平均分成两组,对照组和前庭损毁组,双侧鼓室内注射4-氨基苯砷酸钠(100 g/L)以损毁内耳迷路感受器。两组动物均经过2h双轴旋转运动刺激后,取含Pa的脑块并进行冠状切片(25μm)。以亲和素-生物素过氧化物酶体系(ABC)法对切片进行Fos蛋白免疫组织化学染色,观察和统计学分析Pa内Fos阳性神经元数量变化。结果药物损毁前庭后,动物头部有左右摇晃,运动时身体不稳或转圈等不平衡现象。免疫组织化学结果显示,两组动物下丘脑多个区域有大量Fos阳性神经元出现,其中Pa、室周核以及下丘脑外侧部等区域Fos阳性神经元密度更高。统计学分析表明,前庭损毁组动物Pa内Fos阳性神经元数目较正常组动物显著降低(P〈0.05),其中对照组为(104.00±7.00)个,前庭损毁组为(62.67±7.06)个。结论前庭信息传入能够激活Pa神经元,提示Pa神经元在前庭信息引发的自主反应中发挥一定的作用。
Objective To investigate the activation of paraventricular hypothalamic nucleus (Pa) neurons in response to motion stimulation of venstibular end organs in order to explore the role of Pa in vestibular-autonomic responses and the neural mechanism therein. Methods A total of ten male Sprague-Dawley (SD) rats were equally divided into two groups, i.e. control and vestibular lesion groups. Sodium 4-aminophenylarsonate (100 g/L ) was injected bilaterally into tympanic cavities to destroy the labyrinth of inner ear. After 2 hours-motion stimulation by double-axes rotation for two groups of animals, brain blocks containing Pa were removed and cut coronally into slices of 25μm thick. The sections were then processed for Fos protein immunostaining by avidin-biotin complex (ABC) method before examination, quantification and statistical analysis of Fos-positive neurons in Pa. Results Successful chemical labyrinthectomy induced body imbalance presenting with head jerking or trembling rock from side to side, shaking and unstable or circular walking behaviours. Immunohistochemical staining showed a great number of Fos-postive neurons in several regions of Pa, with higher staining density observed in Pa, periventricular hypothalamic nucleus and lateral hypothalamus. Statistical analysis demonstrates that Fos-positive neurons in Pa, as compared with those in normal animals, were significantly reduced in animals of vestibular lesion group ( P 〈 0.05 ) , represented by 104. 00 ± 7.00 and 62.67 ±7.06 for normal and lesioned animals, respectively. Conclusion Vestibular signal activates Pa neurons, suggesting that Pa neurons play specific roles in generation of vestibular-autonomic responses.