NEURONAL ELEMENTS THAT MEDIATE ESCAPE SWIMMING AND SUPPRESS FEEDING-BEHAVIOR IN THE PREDATORY SEA SLUG PLEUROBRANCHAEA
NEURONAL ELEMENTS THAT MEDIATE ESCAPE SWIMMING AND SUPPRESS FEEDING-BEHAVIOR IN THE PREDATORY SEA SLUG PLEUROBRANCHAEA
复制标题
DOI：
10.1152/jn.1995.74.5.1900
复制
发表时间：
1995-11-01
影响因子：
2.5
通讯作者：
GILLETTE, R
中科院分区：
文献类型：
--
作者：
JING, J;GILLETTE, R
1.白色，双侧成对的A1中间神经元的胸膜神经节的Pleurobranchaea californica火灾有节奏的动作电位爆发在逃避游泳行为。我们研究了A1 s在整体动物和离体中枢神经系统动物游泳行为和模式生成中的作用.逃避游泳是身体的背侧和腹侧屈曲的循环序列。在游泳过程中，A1爆发之前，并伴随着背屈阶段的周期。超极化的A1，以防止尖峰活动中断游泳行为在整个动物和虚构的游泳在孤立的中枢神经系统。未观察到刺激的A1活性引起整个动物的游泳，并且仅偶尔足以在分离的CNS中触发虚构的游泳活动。在静止的整个动物制备中，刺激单个A1通常引起单个背侧屈曲，然后身体屈曲到受刺激细胞的对侧;特征性地，A1尖峰活动刺激反馈抑制，与背侧屈曲的结束和对侧屈曲的开始一致。A1尖峰活动抑制进食行为，并导致整个动物准备诱导喂养的长鼻回缩。A1活性还抑制由刺激分离的中枢神经系统中进食运动网络的关键阶段脑旁神经元（PC（p）s）驱动的虚构进食。同时，A1峰电位对PCp中间神经元产生强抑制作用。A1 s特异性地被有害的机械和化学刺激所兴奋，但不受进食刺激或进食行为的发生的影响。我们的结论是，A1神经元的逃生游泳模式发电机的元素，他们可能是同源的裸鳃Tritonia diomedea类似的C2神经元。除了产生游泳模式之外，它们的功能之一可能是抑制对有害刺激的摄食行为。这些观察结果提供了一个神经机制的原始观察的优势，逃生游泳行为喂养。
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 (PC(p)s) 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.