Kemenes G, Elliott C J
Department of Biology, University of York, Heslington, United Kingdom.
J Neurosci. 1994 Jan;14(1):153-66. doi: 10.1523/JNEUROSCI.14-01-00153.1994.
We have photoinactivated identified feeding interneurons known as N1 and N2 neurons. These are pattern-generating neurons that are active in the protraction of the radula and rasping phases, respectively, of the feeding cycle of the pond snail. The N1 or N2 feeding interneurons in the buccal ganglia were filled with the fluorescent dye 5(6)-carboxyfluorescein (5-CF) from the cut end of the nerve that contains their axon. Filling the cerebrobuccal connective (N = 151) stained just one N1 cell in the contralateral buccal ganglion. Filling the postbuccal nerve stained neurons symmetrically in both buccal ganglia (N = 75): only one labeled cell in each ganglion is an N2 interneuron. The feeding rhythm was evoked by depolarizing a modulatory neuron, the SO, located in the buccal ganglia. The axonally filled N1 interneuron was irradiated at its axon in the buccal commissure with blue laser light (intensity of 0.5 MW.m-2). Irradiation of just one N1 completely blocked the feeding rhythm (seven preparations). In seven further preparations, N1 ablation slowed the SO-driven feeding rhythm and weakened the N1 input to the feeding neurons. Irradiation of the cell bodies of both the filled left and right N2 interneurons killed the cells but did not produce any consistent change in the feeding rate (15 preparations). The feeding interneurons and motoneurons still showed the characteristic N2 phase synaptic inputs, so more, as yet unidentified, N2 neurons must be located in other parts of the buccal ganglia. We conclude that the participation of the identified N1 interneurons is essential for the normal feeding pattern while other, still to be identified N2 neurons must be present and must contribute to the feeding rhythm. We suggest that the extra redundancy of the N2 network may be related to the greater necessity of sensory feedback control during rasping than during protraction of the radula.
我们用光灭活了已鉴定的摄食中间神经元，即N1和N2神经元。这些是模式生成神经元，分别在池塘蜗牛摄食周期的齿舌伸出和锉磨阶段活跃。通过从包含其轴突的神经的切断端向颊神经节中的N1或N2摄食中间神经元填充荧光染料5(6)-羧基荧光素（5-CF）。填充脑颊连接（N = 151）仅使对侧颊神经节中的一个N1细胞染色。填充颊后神经使两个颊神经节中的神经元对称染色（N = 75）：每个神经节中只有一个标记细胞是N2中间神经元。通过使位于颊神经节中的调节神经元SO去极化来诱发摄食节律。用蓝色激光（强度为0.5 MW.m-2）在颊连合处对轴突填充的N1中间神经元的轴突进行照射。仅照射一个N1就完全阻断了摄食节律（七个标本）。在另外七个标本中，N1切除减缓了SO驱动的摄食节律，并减弱了N1对摄食神经元的输入。对填充的左右N2中间神经元的细胞体进行照射杀死了细胞，但摄食速率没有产生任何一致的变化（15个标本）。摄食中间神经元和运动神经元仍然显示出特征性的N2阶段突触输入，因此，更多尚未鉴定的N2神经元必定位于颊神经节的其他部位。我们得出结论，已鉴定的N1中间神经元的参与对于正常摄食模式至关重要，而其他尚未鉴定的N2神经元必定存在并且必定对摄食节律有贡献。我们认为，N2网络的额外冗余可能与锉磨期间比齿舌伸出期间更大的感觉反馈控制必要性有关。
