Serrano Geidy E, Miller Mark W
Institute of Neurobiology and Department of Anatomy, University of Puerto Rico, San Juan, Puerto Rico.
J Neurophysiol. 2006 Oct;96(4):2056-71. doi: 10.1152/jn.00282.2006. Epub 2006 May 31.
This investigation examined the activity of a bilateral pair of motor neurons (B67) in the feeding system of Aplysia californica. In isolated ganglia, B67 firing exhibited a highly stereotyped bursting pattern that could be attributed to an underlying TTX-resistant driver potential (DP). Under control conditions, this bursting in the two B67 neurons was infrequent, irregular, and asynchronous. However, bath application of the neuromodulator dopamine (DA) increased the duration, frequency, rhythmicity, and synchrony of B67 bursts. In the absence of DA, depolarization of B67 with injected current produced rhythmic bursting. Such depolarization-induced rhythmic burst activity in one B67, however, did not entrain its contralateral counterpart. Moreover, when both B67s were depolarized to potentials that produced rhythmic bursting, their synchrony was significantly lower than that produced by DA. In TTX, dopamine increased the DP duration, enhanced the amplitude of slow signaling between the two B67s, and increased DP synchrony. A potential source of dopaminergic signaling to B67 was identified as B65, an influential interneuron with bilateral buccal projections. Firing B65 produced bursts in the ipsilateral and contralateral B67s. Under conditions that attenuated polysynaptic activity, firing B65 evoked rapid excitatory postsynaptic potentials in B67 that were blocked by sulpiride, an antagonist of synaptic DA receptors in this system. Finally, firing a single B65 was capable of producing a prolonged period of rhythmic synchronous bursting of the paired B67s. It is proposed that modulatory dopaminergic signaling originating from B65 during consummatory behaviors can promote rhythmicity and bilateral synchrony in the paired B67 motor neurons.
本研究考察了加州海兔摄食系统中一对双侧运动神经元（B67）的活动。在分离的神经节中，B67放电呈现出高度刻板的爆发模式，这可归因于一种潜在的对河豚毒素（TTX）不敏感的驱动电位（DP）。在对照条件下，两个B67神经元的这种爆发不频繁、不规则且不同步。然而，浴用神经调质多巴胺（DA）增加了B67爆发的持续时间、频率、节律性和同步性。在没有DA的情况下，通过注入电流使B67去极化会产生节律性爆发。然而，一个B67中这种去极化诱导的节律性爆发活动并不会带动其对侧的B67。此外，当两个B67都去极化到产生节律性爆发的电位时，它们的同步性明显低于DA产生的同步性。在TTX存在的情况下，多巴胺增加了DP的持续时间，增强了两个B67之间慢信号的幅度，并增加了DP的同步性。已确定向B67传递多巴胺能信号的一个潜在来源是B65，它是一个有影响力的中间神经元，有双侧颊部投射。激发B65会在同侧和对侧的B67中产生爆发。在减弱多突触活动的条件下，激发B65会在B67中诱发快速兴奋性突触后电位，该电位可被舒必利阻断，舒必利是该系统中突触DA受体的拮抗剂。最后，激发单个B65能够使成对的B67产生长时间的节律性同步爆发。有人提出，在进食行为期间，源自B65的调节性多巴胺能信号可促进成对的B67运动神经元的节律性和双侧同步性。
