GRUNDFEST H, REUBEN J P, RICKLES W H
J Gen Physiol. 1959 Jul 20;42(6):1301-23. doi: 10.1085/jgp.42.6.1301.
Effects of drugs on resting potential, membrane resistance, and excitatory and inhibitory postsynaptic potentials (e.p.s.p.'s and i.p.s.p.'s) of lobster muscle fibers were studied using intracellular microelectrodes Acetylcholine, d-tubocurarine, strychnine, and other drugs of respectively related actions on vertebrate synapses were without effects even in 1 per cent solutions (10(-)w/v). Gamma-aminobutyric acid (GABA) acted powerfully and nearly maximally at 10(-7) to 10(-6)w/v. Membrane resistance fell two- to tenfold, the resting potential usually increasing slightly. This combination of effects, which indicates activation of inhibitory synaptic membrane, was also produced by other short chain omega-amino acids and related compounds that inactivate depolarizing axodendritic synapses of cat. The conductance change, involving increased permeability to Cl(-), by its clamping action on membrane potential shortened as well as decreased individual e.p.s.p.'s. Picrotoxin in low concentration (ca. 10(-7)w/v) and guanidine in higher (ca. 10(-3)w/v) specifically inactivate inhibitory synapses. GABA and picrotoxin are competitive antagonists. The longer chain omega-amino acids which inactivate hyperpolarizing axodendritic synapses of cat are without effect on lobster neuromuscular synapse. However, one member of this group, carnitine (beta-OH-GABA betaine), activated the excitatory synapses, a decreased membrane resistance being associated with depolarzation. The pharmacological properties of lobster neuromuscular synapses and probably also of other crustacean inhibitory synapses appear to stand in a doubly inverted relation to axodendritic synapses of cat.
利用细胞内微电极研究了药物对龙虾肌肉纤维静息电位、膜电阻以及兴奋性和抑制性突触后电位（兴奋性突触后电位和抑制性突触后电位）的影响。乙酰胆碱、d -筒箭毒碱、士的宁以及其他对脊椎动物突触有相应作用的药物，即使在1%的溶液（10⁻² w/v）中也没有效果。γ-氨基丁酸（GABA）在10⁻⁷至10⁻⁶ w/v时作用强烈且接近最大效应。膜电阻下降两到十倍，静息电位通常略有增加。这种效应组合表明抑制性突触膜被激活，其他短链ω-氨基酸和相关化合物也会产生这种效应，这些化合物会使猫的去极化轴突树突突触失活。电导变化涉及对Cl⁻的通透性增加，通过其对膜电位的钳制作用，缩短并降低了单个兴奋性突触后电位。低浓度（约10⁻⁷ w/v）的印防己毒素和高浓度（约10⁻³ w/v）的胍特异性地使抑制性突触失活。GABA和印防己毒素是竞争性拮抗剂。使猫的超极化轴突树突突触失活的长链ω-氨基酸对龙虾神经肌肉突触没有影响。然而，该组中的一个成员肉碱（β-OH - GABA甜菜碱）激活了兴奋性突触，膜电阻降低与去极化相关。龙虾神经肌肉突触以及可能其他甲壳类动物抑制性突触的药理学特性似乎与猫的轴突树突突触呈双重倒置关系。
