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Neurochemical Architecture of the Central Complex Related to Its Function in the Control of Grasshopper Acoustic Communication

机译:中央复合物的神经化学结构与其在蚱hopper声通信中的功能有关

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摘要

The central complex selects and coordinates the species- and situation-specific song production in acoustically communicating grasshoppers. Control of sound production is mediated by several neurotransmitters and modulators, their receptors and intracellular signaling pathways. It has previously been shown that muscarinic cholinergic excitation in the central complex promotes sound production whereas both GABA and nitric oxide/cyclic GMP signaling suppress its performance. The present immunocytochemical and pharmacological study investigates the question whether GABA and nitric oxide mediate inhibition of sound production independently. Muscarinic ACh receptors are expressed by columnar output neurons of the central complex that innervate the lower division of the central body and terminate in the lateral accessory lobes. GABAergic tangential neurons that innervate the lower division of the central body arborize in close proximity of columnar neurons and thus may directly inhibit these central complex output neurons. A subset of these GABAergic tangential neurons accumulates cyclic GMP following the release of nitric oxide from neurites in the upper division of the central body. While sound production stimulated by muscarine injection into the central complex is suppressed by co-application of sodium nitroprusside, picrotoxin-stimulated singing was not affected by co-application of this nitric oxide donor, indicating that nitric oxide mediated inhibition requires functional GABA signaling. Hence, grasshopper sound production is controlled by processing of information in the lower division of the central body which is subject to modulation by nitric oxide released from neurons in the upper division.
机译:中央建筑群在传声蚱grass中选择并协调特定物种和特定情况下的歌曲制作。声音产生的控制是由几种神经递质和调节剂,它们的受体和细胞内信号传导途径介导的。以前已经表明,中央复合物中的毒蕈碱胆碱能激发促进声音产生,而GABA和一氧化氮/环状GMP信号均抑制其性能。目前的免疫细胞化学和药理研究调查了GABA和一氧化氮是否独立介导声音产生抑制的问题。毒蕈碱型ACh受体由中枢复合体的柱状输出神经元表达,该神经元支配中枢体的下部,并终止于侧副叶。支配中央身体下半部的GABA能切向神经元在柱状神经元的附近紧密乔化,因此可能直接抑制这些中央复合输出神经元。这些GABA能切向神经元的一个子集在中央体上半部的神经突释放一氧化氮后累积GMP循环。虽然通过共同施用硝普钠抑制了毒蕈碱注射到中央复合物中而刺激的声音产生,但通过同时施用这种一氧化氮供体不会影响微毒素刺激的歌唱,这表明一氧化氮介导的抑制作用需要功能性GABA信号传导。因此,蚱sound声音的产生是通过处理中央主体下部的信息来控制的,该信息受到上部神经元释放的一氧化氮的调节。

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