O'Gara B A, Friesen W O
Department of Biological Sciences, Barnard College of Columbia University, New York, NY 10027, USA.
J Comp Physiol A. 1995 Nov;177(5):627-36. doi: 10.1007/BF00207191.
Cell Tr2 is a neuron in the subesophageal ganglion of the leech that can trigger swim episodes. In this report, we describe the ability of Tr2 to terminate ongoing swim episodes as well as to trigger swimming. Stimulation of Tr2 terminated ongoing swim episodes in nearly every preparation tested, while Tr2 stimulation triggered swim episodes in only a minority of the preparations. We suggest that the primary role of Tr2 is in the termination rather than the initiation of swimming activity. The swim trigger neuron Tr3 and a swim-gating neuron, cell 21, hyperpolarized during Tr2-induced swim termination. Another swim-gating neuron, cell 204 was sometimes slightly excited, but more often, hyperpolarized during Tr2-induced swim termination. In contrast to these cells, Tr2 stimulation excited another swim-gating neuron, cell 61. The responses of the swim-gating cells were variable in amplitude and sometimes not evident during Tr2-induced swim termination. Hence, the effects of Tr2 stimulation on swim-gating neurons seem unlikely to be the direct cause of swim termination. Oscillator cells examined during Tr2-induced swim termination include: 27, 28, 33, 60, 115, and 208. The largest effect seen in an oscillator neuron was in cell 208, which was repolarized by up to 10 mV during Tr2 stimulation. Tr2 stimulation did not produce any obvious synaptic effects in motor neurons DI-1, VI-1, and DE-3. Our findings indicate that other, yet undiscovered, connections are likely to be important in Tr2-induced swim termination. Therefore, we propose that cell Tr2 is probably a member of a distributed neural network involved in swim termination.
细胞Tr2是水蛭咽下神经节中的一种神经元,能够触发游泳行为。在本报告中,我们描述了Tr2终止正在进行的游泳行为以及触发游泳的能力。在几乎所有测试的标本中,刺激Tr2都能终止正在进行的游泳行为,而刺激Tr2仅在少数标本中能触发游泳行为。我们认为Tr2的主要作用是终止而非启动游泳活动。游泳触发神经元Tr3和一个游泳门控神经元细胞21在Tr2诱导的游泳终止过程中发生超极化。另一个游泳门控神经元细胞204有时会稍有兴奋,但在Tr2诱导的游泳终止过程中更常发生超极化。与这些细胞不同,刺激Tr2会使另一个游泳门控神经元细胞61兴奋。在Tr2诱导的游泳终止过程中,游泳门控细胞的反应幅度各不相同,有时并不明显。因此,Tr2刺激对游泳门控神经元的影响似乎不太可能是游泳终止的直接原因。在Tr2诱导的游泳终止过程中检测的振荡细胞包括:27、28、33、60、115和208。在振荡神经元中观察到的最大效应出现在细胞208中,在Tr2刺激期间其复极化高达10 mV。Tr2刺激在运动神经元DI-1、VI-1和DE-3中未产生任何明显的突触效应。我们的研究结果表明,其他尚未发现的连接在Tr2诱导的游泳终止中可能很重要。因此,我们提出细胞Tr2可能是参与游泳终止的分布式神经网络的一员。