Glutamate as an inhibitory transmitter in the crayfish local circuit

通过电生理、形态学、药理学和神经化学分析，揭示了GABA和谷氨酸在控制克氏原螯虾尾足运动的腹终节局部回路神经元之间的突触相互作用中起抑制神经递质作用。控制尾足运动的局部回路由上行节间神经元、刺突局部神经元和非刺突局部神经元组成，支配尾扇毛发的机械感觉传入的感觉信息通过这些局部回路神经元传递给支配尾足肌肉的运动神经元。双标记法结合细胞内路西法黄染色和谷氨酸免疫细胞化学染色表明，支配尾足和端子的许多运动神经元和一些局部尖峰间神经元是谷氨酸能的。许多局部回路神经元对GABA和谷氨酸的局部压力喷射都表现出抑制反应和膜超极化，尾足运动神经元对感觉刺激的抑制反应是由GABA介导的，因为由感觉刺激或GABA喷射引起的运动神经元的膜超极化不受微毒素（PTX）的影响，尽管运动膜超极化的幅度很大由谷氨酸介导的神经元被PTX反向减少。因此，非尖峰局部中间神经元的膜超极化似乎是由非尖峰局部中间神经元释放的GABA和尖峰局部中间神经元释放的谷氨酸介导的。

Not only GABA but also glutamate is revealed to act as an inhibitory neurotransmitter at synaptic interactions between local circuit neurones in the terminal abdominal ganglion that is a centre controlling uropod movements of the crayfish Procambarus clarkii Girard by using electrophysiological, morphological, pharmacological and neurochemical analyzes. Local circuit controlling uropod movements is consisted of ascending intersegmental interneurones, spiking local interneurones and nonspiking local interneurones and sensory information from the mechanosensory afferents innervating hairs on the tailfan is transmitted to the motor neurones innervating uropod muscles via these local circtrit neurones. Double labelling method that is a combination of intracellular staining with Lucifer yellow and immunocytochemical staining against glutamate suggested many motor neurones innervating the uropods and the telson and some spiking local interneurones were glutamatergic. Many local circuit neurones showed inhibitory response and were hyperpolarized their membrane in response to local pressure ejection of both GABA and glutamate and the inhibitory response of the uropod motor neurones to the sensory stimulation was mediated by GABA since membrane hyperpolarization of the motor neurones induced by either sensory stimulation or GABA ejection was unaffected by bath application of picrotoxin (PTX) although the amplitude of membrane hyperpolarization of the motor neurones mediated by glutamate was reversely reduced by PTX. Membrane hyperpolarization of the nonspiking local interneurones was therefore seemed to mediate by both GABA released from the nonspiking local interneurones and glutamate released from spiking local interneurones.