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进食刺激物激活一种已确定的多巴胺能中间神经元,该神经元诱导椎实螺的进食运动程序。

Feeding stimulants activate an identified dopaminergic interneuron that induces the feeding motor program in Helisoma.

作者信息

Quinlan E M, Arnett B C, Murphy A D

机构信息

Department of Biological Sciences, University of Illinois at Chicago, 60607, USA.

出版信息

J Neurophysiol. 1997 Aug;78(2):812-24. doi: 10.1152/jn.1997.78.2.812.

Abstract

The neurotransmitter dopamine is shown to play a fundamental role in the generation of the feeding motor pattern and resultant feeding behavior in Helisoma. Application of exogenous dopamine triggered the fictive feeding motor pattern in the isolated CNS and triggered feeding movements in semi-intact preparations. Application of feeding stimulants to the oral cavity excited the putatively dopaminergic buccal interneuron N1a, and depolarization of interneuron N1a triggered the production of the fictive feeding motor pattern. The ability of dopamine superfusion and of interneuron N1a stimulation to activate the fictive feeding motor pattern was blocked by the dopamine antagonist sulpiride. The phase of the fictive feeding motor pattern was reset by brief hyperpolarization of interneuron N1a, demonstrating that interneuron N1a is an integral component of the buccal central pattern generator (CPG). During spontaneous fictive feeding patterns, prolonged hyperpolarizations of interneuron N1a inhibited the production of patterned activity. Exogenous dopamine maintained the fictive feeding motor pattern in the absence of interneuron N1a activity. Interneuron N1a was labeled by the formaldehyde-glutaraldehyde histochemical technique, which is indicative of the presence of dopamine in mollusks. These data suggest that interneuron N1a is an endogenous source of the neuromodulator dopamine, intrinsic to the buccal CPG, and that interneuron N1a has a prominent role in the sensory-motor integration triggering the consummatory response.

摘要

已证明神经递质多巴胺在椎实螺进食运动模式的产生及由此产生的进食行为中发挥着重要作用。外源性多巴胺的应用在分离的中枢神经系统中触发了虚构的进食运动模式,并在半完整制剂中触发了进食运动。将进食刺激物应用于口腔会兴奋假定为多巴胺能的颊中间神经元N1a,中间神经元N1a的去极化会触发虚构进食运动模式的产生。多巴胺拮抗剂舒必利可阻断多巴胺超融合和中间神经元N1a刺激激活虚构进食运动模式的能力。中间神经元N1a的短暂超极化会重置虚构进食运动模式的相位,这表明中间神经元N1a是颊中央模式发生器(CPG)的一个组成部分。在自发的虚构进食模式期间,中间神经元N1a的长时间超极化会抑制模式化活动的产生。在没有中间神经元N1a活动的情况下,外源性多巴胺维持了虚构进食运动模式。中间神经元N1a通过甲醛 - 戊二醛组织化学技术标记,这表明软体动物中存在多巴胺。这些数据表明,中间神经元N1a是颊CPG固有的神经调质多巴胺的内源性来源,并且中间神经元N1a在触发 consummatory反应的感觉运动整合中起重要作用。

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