Gutovitz S, Birmingham J T, Luther J A, Simon D J, Marder E
Volen Center and Biology Department, Brandeis University, Waltham, Massachusetts 02454-9110, USA.
J Neurosci. 2001 Aug 15;21(16):5935-43. doi: 10.1523/JNEUROSCI.21-16-05935.2001.
GABA mediates both presynaptic and postsynaptic inhibition at many synapses. In contrast, we show that GABA enhances transmission at excitatory synapses between the lateral gastric and medial gastric motor neurons and the gastric mill 6a and 9 (gm6a, gm9) muscles and between the lateral pyloric motor neuron and pyloric 1 (p1) muscles in the stomach of the lobster Homarus americanus. Two-electrode current-clamp or voltage-clamp techniques were used to record from muscle fibers. The innervating nerves were stimulated to evoke excitatory junctional potentials (EJPs) or excitatory junctional currents. Bath application of GABA first decreased the amplitude of evoked EJPs in gm6a and gm9 muscles, but not the p1 muscle, by activating a postjunctional conductance increase that was blocked by picrotoxin. After longer GABA applications (5-15 min), the amplitudes of evoked EJPs increased in all three muscles. This increase persisted in the presence of picrotoxin. beta-(Aminomethyl)-4-chlorobenzenepropanoic acid (baclofen) was an effective agonist for the GABA-evoked enhancement but did not increase the postjunctional conductance. Muscimol activated a rapid postsynaptic conductance but did not enhance the amplitude of the nerve-evoked EJPs. GABA had no effect on iontophoretic responses to glutamate and decreased the coefficient of variation of nerve-evoked EJPs. In the presence or absence of tetrodotoxin, GABA increased the frequency but not the amplitude of miniature endplate potentials. These data suggest that GABA acts presynaptically via a GABA(B)-like receptor to increase the release of neurotransmitter.
γ-氨基丁酸（GABA）在许多突触处介导突触前抑制和突触后抑制。相比之下，我们发现，在美洲螯龙虾的胃中，GABA增强了外侧胃运动神经元和内侧胃运动神经元与胃磨6a和9（gm6a、gm9）肌肉之间以及外侧幽门运动神经元和幽门1（p1）肌肉之间兴奋性突触的传递。采用双电极电流钳或电压钳技术记录肌肉纤维的电活动。刺激支配神经以诱发兴奋性接头电位（EJP）或兴奋性接头电流。浴槽中施加GABA首先通过激活被印防己毒素阻断的接头后电导增加，降低了gm6a和gm9肌肉中诱发EJP的幅度，但对p1肌肉没有影响。在较长时间（5 - 15分钟）施加GABA后，所有三块肌肉中诱发EJP的幅度均增加。在存在印防己毒素的情况下，这种增加仍然持续。β-（氨甲基）-4-氯苯丙酸（巴氯芬）是GABA诱发增强作用的有效激动剂，但不会增加接头后电导。蝇蕈醇激活快速的突触后电导，但不会增强神经诱发EJP的幅度。GABA对谷氨酸离子电泳反应没有影响，并降低了神经诱发EJP的变异系数。在存在或不存在河豚毒素的情况下，GABA增加了微小终板电位的频率，但没有增加其幅度。这些数据表明，GABA通过类GABA(B)受体在突触前起作用，以增加神经递质的释放。
