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在捕食性海蛞蝓侧鳃中介导逃避游泳并抑制摄食行为的神经元成分。

Neuronal elements that mediate escape swimming and suppress feeding behavior in the predatory sea slug Pleurobranchaea.

作者信息

Jing J, Gillette R

机构信息

Department of Physiology, University of Illinois at Urbana-Champaign 61801, USA.

出版信息

J Neurophysiol. 1995 Nov;74(5):1900-10. doi: 10.1152/jn.1995.74.5.1900.

DOI:10.1152/jn.1995.74.5.1900
PMID:8592183
Abstract
  1. The white, bilaterally paired A1 interneurons of the cerebropleural ganglion of Pleurobranchaea californica fire rhythmic bursts of action potentials during escape swimming behavior. We studied the role of the A1s in swimming behavior and pattern generation in whole animal and isolated CNS preparations. 2. The escape swim is a cyclic sequence of dorsal and ventral flexions of the body. During the swim, A1 bursts precede and accompany the dorsal flexion phase of the cycle. Hyperpolarization of A1 to prevent spike activity interrupts swimming behavior in the whole animal and fictive swimming in the isolated CNS. Stimulated A1 activity was not observed to cause swimming in whole animals, and was only occasionally sufficient to trigger fictive swimming activity in the isolated CNS. 3. In quiescent whole animal preparations, stimulation of a single A1 normally causes a single dorsal flexion followed by body flexion to the side contralateral to the stimulated cell; characteristically, A1 spike activity stimulates feedback inhibition coinciding with the end of dorsal flexion and the onset of contralateral flexion. 4. A1 spike activity suppresses feeding behavior and causes proboscis retraction in whole animal preparations induced to feed. A1 activity also suppresses fictive feeding driven by stimulation of the critical phasic paracerebral neurons (PCps) of the motor network of feeding in the isolated CNS. Concomitantly, A1 spikes cause potent inhibition of the PCp interneurons. 5. The A1s are specifically excited by noxious mechanical and chemical stimuli, but are not affected by feeding stimuli or the occurrence of feeding behavior. 6. We conclude that the A1 neurons are elements of an escape swimming pattern generator, and that they are probably homologous to the similar C2 neurons of the nudibranch Tritonia diomedea. One of their functions outside of generating the swim pattern may be the suppression of feeding behavior in response to noxious stimulation. These observations provide a neural mechanism for the original observations of the dominance of escape swimming behavior over feeding.
摘要
  1. 加州侧鳃海蛞蝓脑胸膜神经节中白色的、双侧成对的A1中间神经元在逃避游泳行为期间会产生有节奏的动作电位爆发。我们在完整动物和离体中枢神经系统制剂中研究了A1中间神经元在游泳行为和模式生成中的作用。2. 逃避游泳是身体背腹弯曲的循环序列。在游泳过程中,A1爆发先于并伴随循环的背屈阶段。对A1进行超极化以防止动作电位活动会中断完整动物的游泳行为以及离体中枢神经系统中的虚拟游泳。未观察到刺激A1活动会在完整动物中引发游泳,并且仅偶尔足以在离体中枢神经系统中触发虚拟游泳活动。3. 在静止的完整动物制剂中,刺激单个A1通常会导致单次背屈,随后身体向受刺激细胞对侧弯曲;其特征是,A1动作电位活动会刺激反馈抑制,与背屈结束和对侧弯曲开始同时发生。4. A1动作电位活动会抑制完整动物制剂中的进食行为并导致吻部回缩,这些制剂被诱导进食。A1活动还会抑制由离体中枢神经系统中进食运动网络的关键相位脑旁神经元(PCps)刺激驱动的虚拟进食。同时,A1动作电位会强烈抑制PCp中间神经元。5. A1中间神经元会被有害的机械和化学刺激特异性兴奋,但不受进食刺激或进食行为发生的影响。6. 我们得出结论,A1神经元是逃避游泳模式发生器的组成部分,并且它们可能与裸鳃类动物多氏海神鳃的类似C2神经元同源。它们在产生游泳模式之外的功能之一可能是响应有害刺激抑制进食行为。这些观察结果为最初关于逃避游泳行为优于进食行为的观察提供了一种神经机制。

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