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Integration of Vestibular and Gastrointestinal Inputs by CerebellarFastigial Nucleus Neurons: Multisensory Influences on MotionSickness

机译:小脑整合前庭和胃肠道输入小脑顶核神经元:对运动的多感官影响。疾病

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摘要

Previous studies demonstrated that ingestion of the emetic compound copper sulfate (CuSO4) alters the responses to vestibular stimulation of a large fraction of neurons in brainstem regions that mediate nausea and vomiting, thereby affecting motion sickness susceptibility. Other studies suggested that the processing of vestibular inputs by cerebellar neurons plays a critical role in generating motion sickness, and that neurons in the cerebellar fastigial nucleus receive visceral inputs. These findings raised the hypothesis that stimulation of gastrointestinal receptors by a nauseogenic compound affects the processing of labyrinthine signals by fastigial nucleus neurons. We tested this hypothesis in decerebrate cats by determining the effects of intragastric injection of CuSO4 on the responses of rostral fastigial nucleus to whole-body rotations that activate labyrinthine receptors. Responses to vestibular stimulation of fastigial nucleus neurons were more complex in decerebrate cats than reported previously in conscious felines. In particular, spatiotemporal convergence (STC) responses, which reflect the convergence of vestibular inputs with different spatial and temporal properties, were more common in decerebrate than in conscious felines. The firing rate of a smallpercentage of fastigial nucleus neurons (15%) was altered over50% by the administration of CuSO4; the firing rate of themajority of these cells decreased. The responses to vestibular stimulation of amajority of these cells were attenuated after the compound was provided.Although these data support our hypothesis, the low fraction of fastigialnucleus neurons whose firing rate and responses to vestibular stimulation wereaffected by the administration of CuSO4 cast doubt on the notion thatnauseogenic visceral inputs modulate motion sickness susceptibility principallythrough neural pathways that include the cerebellar fastigial nucleus. Instead,it appears that convergence of gastrointestinal and vestibular inputs occursmainly in the brainstem.
机译:先前的研究表明,摄入催吐化合物硫酸铜(CuSO4)会改变对介导恶心和呕吐的脑干区域中大部分神经元的前庭刺激的反应,从而影响晕动病的易感性。其他研究表明,小脑神经元对前庭输入的处理在产生晕动病中起关键作用,而小脑小脑顶核中的神经元接受内脏输入。这些发现提出了这样的假说:由恶心的化合物刺激胃肠道受体会影响小肠​​核神经元对迷宫信号的处理。我们通过确定胃内注射CuSO4对鸟嘴状小脑顶核对激活迷宫受体的全身旋转的反应的影响,在去脑猫中测试了这一假设。去脑猫对前庭神经对前庭核神经元的刺激反应比先前在有意识的猫科动物中报道的更为复杂。特别地,时空会聚(STC)反应反映出具有不同时空特性的前庭输入的会聚,在无脑动物中比在有意识的猫科动物中更常见。射速小小脑顶核神经元的百分比(15%)硫酸铜的50%;的发射率这些细胞大多数减少。对前庭刺激的反应提供化合物后,这些细胞中的大多数已减毒。尽管这些数据支持了我们的假设,但假牙的比例很低核神经元的放电率和对前庭刺激的反应为受硫酸铜管理影响的观念恶心内脏输入主要调节晕动病易感性通过包括小脑小脑顶核的神经通路。代替,似乎发生了胃肠道和前庭输入的融合主要在脑干。

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