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The pharmacological properties of some crustacean neuronal acetylcholine gamma-aminobutyric acid and L-glutamate responses.

机译:某些甲壳类神经元乙酰胆碱γ-氨基丁酸和L-谷氨酸反应的药理特性。

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摘要

1. A study was performed of the L-glutamate, gamma-aminobutyric acid (GABA), and acetylcholine (ACh) responses of cells in the stomatogastric ganglion of the crab, Cancer pagurus. 2. Ionophoretic or pressure application of L-glutamate revealed three classes of responses: a K+-dependent inhibition which reversed at 15-20 mV more negative than the resting potential; a Cl- dependent inhibitory response which was at equilibrium at the resting potential; and a depolarizing response. 3. Ionophoretic or pressure applications of GABA likewise produced three kinds of responses: an increase in K+ conductance, an increase in Cl- conductance, and a depolarizing response. 4. Picrotoxin (10(-6)-10(-5) M) was effective in blocking both the glutamate inhibitory responses. 10(-4) M-picrotoxin, which was necessary to produce a 50% block of the GABA-K+-dependent response, had no effect on the GABA-Cl- response. 5. beta-Guanidinopropionic acid (beta-GP) was found to be an agonist for the GABA-K+ response, but was ineffective in mimicking or blocking the GABA-Cl- response. 6. ACh applications produced large depolarizing responses with a pharmacological profile similar to that of the nicotinic ganglionic response in vertebrates. 7. The muscarinic agonist, acetyl-beta-methyl choline (MeCh), produced depolarizations which decreased in amplitude as the membrane was hyperpolarized from -40 to -100 mV. Pilocarpine and oxotremorine produced changes in the endogenous activity of ganglionic neurones. 8. Implications of these results for the identification of synaptic transmitters in the somatogastric ganglion are discussed.
机译:1.对蟹癌巨蟹座的胃胃神经节中细胞的L-谷氨酸,γ-氨基丁酸(GABA)和乙酰胆碱(ACh)反应进行了研究。 2. L-谷氨酸的离子渗透压或压力施加显示出三类响应:K +依赖性抑制,在15-20 mV处逆转,比静息电位更负。 Cl-依赖性抑制反应,在静息电位处于平衡状态;和去极化反应。 3. GABA的离子透入或压力施加同样产生三种响应:K +电导增加,Cl-电导增加和去极化响应。 4.微毒素(10(-6)-10(-5)M)可有效阻断两种谷​​氨酸抑制反应。 10(-4)M-pictotoxin是产生50%的GABA-K +依赖性应答阻断所必需的,对GABA-Cl-应答无影响。 5.发现β-胍基丙酸(β-GP)是针对GABA-K +应答的激动剂,但是在模仿或阻断GABA-Cl-应答方面无效。 6. ACh的应用产生了很大的去极化反应,其药理学特征与脊椎动物的烟碱神经节反应相似。 7.毒蕈碱激动剂,乙酰基-β-甲基胆碱(MeCh)产生的去极化,随着膜超极化从-40 mV到-100 mV,振幅减小。毛果芸香碱和oxotremorine产生神经节神经元的内源性活动​​的变化。 8.讨论了这些结果对确定体胃神经节中突触递质的意义。

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