Ogawa S, Kow L M, Pfaff D W
Rockefeller University, Department of Neurobiology and Behavior, New York, NY 10021.
Exp Brain Res. 1991;85(1):85-92. doi: 10.1007/BF00229989.
Functional and neurochemical evidence suggests significant GABA participation in the basomedial hypothalamus. We have investigated electrophysiological effects of GABA using in vitro recording from hypothalamic tissue slices. Exogenous GABA inhibited 94 out of 121 ventromedial hypothalamic (VMN) neurons tested. In sixty-one percent of these GABA-responsive neurons, the inhibitory action of GABA was blocked by GABAA antagonists, bicuculline methiodide (BMI) and picrotoxin (PTX). Nevertheless, many (27/69) GABA-responsive neurons were not sensitive to GABAA blockers: BMI and PTX failed to antagonize inhibitory action of GABA. Most, if not all, of these inhibitions can be accounted for by GABAB effects, since baclofen powerfully inhibited 42 of 44 neurons tested. In addition to blocking the inhibitory action of exogenous GABA, BMI (55%) and PTX (36%) also caused changes of neuronal activity indicating blockade of intrinsic GABAergic action. Altogether, our results showed that, in the VMN, GABA acts through not only GABAA but also GABAB receptors to inhibit neuronal activity, and that there is tonic inhibition by intrinsic GABA neurons. These GABA actions may participate in behaviorally-relevant VMN hypothalamic mechanisms.
功能和神经化学证据表明,γ-氨基丁酸(GABA)在基底内侧下丘脑发挥着重要作用。我们利用下丘脑组织切片的体外记录技术,研究了GABA的电生理效应。在所测试的121个腹内侧下丘脑(VMN)神经元中,外源性GABA抑制了94个神经元的活动。在这些对GABA有反应的神经元中,61%的神经元对GABA的抑制作用可被GABAA拮抗剂甲硫酸荷包牡丹碱(BMI)和印防己毒素(PTX)阻断。然而,许多(27/69)对GABA有反应的神经元对GABAA阻滞剂不敏感:BMI和PTX未能拮抗GABA的抑制作用。由于巴氯芬强烈抑制了所测试的44个神经元中的42个,因此这些抑制作用中的大多数(如果不是全部)可归因于GABAB效应。除了阻断外源性GABA的抑制作用外,BMI(55%)和PTX(36%)还引起了神经元活动的变化,表明其阻断了内源性GABA能作用。总之,我们的结果表明,在VMN中,GABA不仅通过GABAA受体,还通过GABAB受体来抑制神经元活动,并且存在内源性GABA神经元的紧张性抑制。这些GABA作用可能参与了与行为相关的VMN下丘脑机制。