Yajima Y, Hayashi Y
Department of Physiology, Hyogo College of Medicine, Japan.
Exp Brain Res. 1990;81(3):581-8. doi: 10.1007/BF02423507.
It is well known that the superficial layers of the dorsal cochlear nucleus (DCN) are rich in GABAergic neurons. We investigated the effects of topical application of GABA receptor agonists and/or antagonists upon the auditory response properties of DCN neurons in rats anesthetized with alpha chloralose-urethane. Auditory stimuli consisted of 20 ms tone bursts presented in a free field. Response properties of DCN neurons were studied before and during iontophoretic application of GABA, bicuculline methiodide (BIC) and muscimol (MUS) alone and GABA with MUS or BIC through triple barrel electrodes glued to the recording microelectrode. Of 68 DCN neurons studied, 27 were sensitive to topical application of the GABA agonists or antagonist. In these neurons, BIC enhanced spontaneous activity as well as auditory responses and decreased the Q-30 quality factor values. MUS reduced auditory responses. BIC often increased the width of the turning curve but GABA and/or MUS reduced it. Without drug application, GABA sensitive neurons tended to have longer response latencies and larger tuning widths at 30 dB above threshold as well as larger Q-30 values as compared with neurons that were insensitive to GABA. These findings suggest that: 1) GABAergic neurons determine the width of the tuning curve in neurons with GABA receptors by curtailing the excitatory response area, and 2) such neurons receive tonic inhibition from intrinsic GABAergic neurons.
众所周知,蜗背侧核(DCN)的浅层富含γ-氨基丁酸(GABA)能神经元。我们研究了局部应用GABA受体激动剂和/或拮抗剂对用α-氯醛糖-乌拉坦麻醉的大鼠DCN神经元听觉反应特性的影响。听觉刺激由自由场中呈现的20毫秒纯音脉冲组成。通过粘贴在记录微电极上的三管电极,在单独离子导入GABA、甲磺酸荷包牡丹碱(BIC)和蝇蕈醇(MUS)以及GABA与MUS或BIC时,研究DCN神经元的反应特性。在所研究的68个DCN神经元中,27个对局部应用GABA激动剂或拮抗剂敏感。在这些神经元中,BIC增强了自发活动以及听觉反应,并降低了Q-30品质因数。MUS降低了听觉反应。BIC通常增加了调谐曲线的宽度,但GABA和/或MUS使其减小。在未应用药物时,与对GABA不敏感的神经元相比,GABA敏感神经元在高于阈值30 dB时往往具有更长的反应潜伏期和更大的调谐宽度以及更大的Q-30值。这些发现表明:1)GABA能神经元通过缩减兴奋性反应区域来决定具有GABA受体的神经元中调谐曲线的宽度,以及2)此类神经元接受来自内在GABA能神经元的紧张性抑制。