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旋转运动刺激前庭感受器激活室旁核神经元活动的形态学证明
Morphological evidence that rotatory stimulation to vestibular end organs activates paraventriclar hypothalamic nucleus neurons
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 vestibularautonomic 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.
室旁核 / 下丘脑 / 前庭感受器 / Fos蛋白 / 免疫组织化学 / 大鼠
Paraventricular hypothalamic nucleus / Hypothalamus / Vestibular end organ / Fos protein / Immunohistochemistry / Rat
［1］Money KE. Motion sickness［J］. Physiol Rev, 1970, 50(1):1-39.
［2］Hornby PJ. Central neurocircuitry associated with emesis［J］. Am J Med, 2001,111 (Suppl 8A):106S-112S.
［3］Abe C, Tanaka K, Iwata C,et al.Vestibular-mediated increase in central serotonin plays an important role in hypergravity-induced hypophagia in rats［J］. J Appl Physiol, 2010, 109(6):1635-1643.
［4］Liu LP, Dong JQ, Zhang ZhCh, et al. Effect of electrolysis of anterior cingulate cortex on motion sickness［J］. Chinese Journal of Neuroanatomy, 2010, 26 (1): 15-19.(in Chinese)
刘立鹏, 董加强, 张卓超, 等.电损毁前扣带回皮质对晕动病的影响 ［J］.神经解剖学杂志, 2010,26(1):15-19.
［5］Horowitz SS, Blanchard J, Morin LP. Medial vestibular connections with the hypocretin (orexin) system ［J］. J Comp Neurol, 2005, 487(2):127-146.
［6］Armstrong WE. Hypothalamic Supraoptic and Paraventricular Nuclei. in George Paxinos. The Rat Nervous System ［M］. 3rd ed. Memphis TN: Elsevier Academic Press, 2004: 369-388.
［7］Herman JP, Cullinan WE. Neurocircuitry of stress: central control of the hypothalamo-pituitary-adrenocortical axis ［J］. Trends Neurosci, 1997, 20(2):78-84.
［8］Suzuki M, Kitano H, Ito R, et al. Cortical and subcortical vestibular response to caloric stimulation detected by functional magnetic resonance imaging ［J］. Brain Res Cogn Brain Res, 2001, 12(3):441-449.
［9］Dieterich M, Brandt T. Functional brain imaging of peripheral and central vestibular disorders ［J］. Brain, 2008, 131(Pt 10):2538-2552.
［10］Pajolla GP, Crippa GE, Corrêa SA, et al. The lateral hypothalamus is involved in the pathway mediating the hypotensive response to cingulate cortex-cholinergic stimulation［J］. Cell Mol Neurobiol, 2001, 21(4):341-356.
［11］Porter JD, Balaban CD. Connections between the vestibular nuclei and brain stem regions that mediate autonomic function in the rat ［J］. J Vestib Res, 1997, 7(1):63-76.
［12］Armstrong WE, Wang L, Li C, et al. Performance, properties, and plasticity of identified xytocin and vasopressin neurones in vitro ［J］. J Neuroendocrinol, 2010, 22(5): 330-342.
［13］Li C, Tripathi PK, Armstrong WE. Differences in spike train variability in rat vasopressin and oxytocin neurons and their relationship to synaptic activity ［J］. J Physiol, 2007,581(Pt1): 221-240.
［14］Li X, Jiang ZL, Wang GH, et al. Plasma vasopressin, an etiologic factor of motion sickness in rat and human ［J］? Neuroendocrinology, 2005, 81(6):351-359.
［15］Maggio N, Segal M. Differential corticosteroid modulation of inhibitory synaptic currents in the dorsal and ventral hippocampus ［J］. J Neurosci, 2009, 29(9):2857-2866.
［16］Arnett MG, Pan MS, Doak W, et al. The role of glucocorticoid receptor-dependent activity in the amygdala central nucleus and reversibility of early-life stress programmed behavior ［J］. Transl Psychiatry, 2015, 5:e542.
［17］Ghosal S, Bundzikova-Osacka J, Dolgas CM,et al. Glucocorticoid receptors in the nucleus of the solitary tract (NTS) decrease endocrine and behavioral stress responses ［J］. Psychoneuroendocrinology, 2014, 45:142-153.
［18］Uno A, Takeda N, Horii A, et al. Effects of amygdala or hippocampus lesion on hypergravity-induced motion sickness in rats ［J］. Acta Otolaryngol, 2000, 120(7):860-865.
［19］Martin S, Henley JM, Holman D, et al. Corticosterone alters AMPAR mobility and facilitates bidirectional synaptic plasticity ［J］. PLoS One, 2009, 4(3):e4714.
［20］Chaouloff F, Hémar A, Manzoni O. Local facilitation of hippocampal metabotropic glutamate receptor-dependent long-term depression by corticosterone and dexamethasone ［J］. Psychoneuroendocrinology, 2008, 33(5):686-691.
前扣带回皮质5HT调节晕动病发生的神经机制;5HT调节易化晕动病的中央杏仁核神经元活动机制研究
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