Chiel H J, Kupfermann I, Weiss K R
Center for Neurobiology and Behavior, New York State Psychiatric Institute, College of Physicians and Surgeons, Columbia University, New York 10032.
J Neurosci. 1988 Jan;8(1):49-63. doi: 10.1523/JNEUROSCI.08-01-00049.1988.
We have identified 2 buccal-cerebral interneurons (BCIs), B17 and B18, that appear to be involved in the coordination of feeding behavior in Aplysia. The BCIs have their cell bodies in the buccal ganglion, but send axons to the cerebral ganglion via the cerebral-buccal connectives. The BCIs appear to make monosynaptic connections with neurons in the cerebral ganglion that modulate extrinsic muscles involved in feeding behavior. B17 and B18 are activated antiphasically during a motor program induced by stimulating the esophageal nerve and appear to "read out" different phases of the buccal program to different cells in the cerebral ganglion. B17 and B18 are not necessary, and probably not sufficient, to generate the buccal program. These BCIs, and other cells like them in the buccal ganglion, may be capable of coordinating the activity of the intrinsic muscles of the buccal mass with the activity of its extrinsic muscles, and perhaps with those of the lips, mouth, and tentacles. Identified histaminergic neuron, C2, can modulate the outputs of the BCIs onto their synaptic followers in the cerebral ganglion. Firing of C2 inhibits spiking of the BCIs, probably via cerebral-buccal interneurons. C2 also decreases the size of the EPSP that B17 and B18 evoke in cerebral neuron C4. C2 appears to do so monosynaptically, and it decreases the conductance of C4, ruling out one possible postsynaptic mechanism of action. Variance analysis of the EPSPs evoked by B18 supports the hypothesis that C2 acts presynaptically to decrease the release of transmitter. Applications of histamine to the solution bathing the neuron mimic the effect of firing C2 and reduce the size of the EPSPs B18 induces in C4. The bath-applied histamine appears to act directly on B18, since it elicits a voltage-dependent increased conductance hyperpolarization recorded in the soma of B18, and the hyperpolarization persists in a solution in which synaptic transmission has been blocked. Histamine did not produce any marked changes of the duration of a TEA-broadened somatic action potential of B18. To the extent that the soma of B18 reflects the membrane properties of its synaptic terminal region, the data suggest that histamine may produce presynaptic inhibition by hyperpolarizing the synaptic terminal region.
我们已经鉴定出2个颊-脑中间神经元（BCIs），即B17和B18，它们似乎参与了海兔进食行为的协调。BCIs的细胞体位于颊神经节，但轴突通过脑-颊连接纤维延伸至脑侧神经节。BCIs似乎与脑侧神经节中的神经元形成单突触连接，这些神经元可调节参与进食行为的外在肌肉。在刺激食管神经诱发的运动程序中，B17和B18呈反相激活，并且似乎向脑侧神经节中的不同细胞“读出”颊部程序的不同阶段。B17和B18对于产生颊部程序并非必需，可能也不充分。这些BCIs以及颊神经节中类似的其他细胞，或许能够协调颊部肌肉内在肌的活动与其外在肌的活动，甚至可能协调唇部、口腔和触手的活动。已鉴定出的组胺能神经元C2，可调节BCIs向其在脑侧神经节中的突触后神经元的输出。C2的放电抑制BCIs的放电，可能是通过脑-颊中间神经元实现的。C2还减小了B17和B18在脑侧神经元C4中诱发的兴奋性突触后电位（EPSP）的幅度。C2似乎是通过单突触起作用的，并且它降低了C4的电导，排除了一种可能的突触后作用机制。对B18诱发的EPSP进行方差分析支持了这样的假说，即C2通过突触前作用来减少递质释放。将组胺应用于浸泡神经元的溶液中，可模拟C2放电的效果，并减小B18在C4中诱发的EPSP的幅度。施加于浴液中的组胺似乎直接作用于B18，因为它在B18的胞体中引发了一种电压依赖性的电导增加的超极化，并且这种超极化在突触传递被阻断的溶液中依然持续。组胺并未使B18的经四乙铵（TEA）展宽的体细胞动作电位的持续时间产生任何显著变化。就B18的胞体反映其突触终末区域的膜特性而言，这些数据表明组胺可能通过使突触终末区域超极化而产生突触前抑制。
