Banks M I, Li T B, Pearce R A
Anesthesiology, University of Wisconsin, Madison, Wisconsin 53706, USA.
J Neurosci. 1998 Feb 15;18(4):1305-17. doi: 10.1523/JNEUROSCI.18-04-01305.1998.
Although two kinetically distinct evoked GABAA responses (GABAA,fast and GABAA,slow) have been observed in CA1 pyramidal neurons, studies of spontaneous IPSCs (sIPSCs) in these neurons have reported only a single population of events that resemble GABAA,fast in their rise and decay kinetics. The absence of slow sIPSCs calls into question the synaptic basis of GABAA,slow. We present evidence here that both evoked responses are synaptic in origin, because two classes of minimally evoked, spontaneous and miniature IPSCs exist that correspond to GABAA,fast and GABAA,slow. Slow sIPSCs occur infrequently, suggesting that the cells underlying these events have a low spontaneous firing rate, unlike the cells giving rise to fast sIPSCs. Like evoked GABAA,fast and GABAA,slow, fast and slow sIPSCs are modulated differentially by furosemide, a subtype-specific GABAA antagonist. Furosemide blocks fast IPSCs by acting directly on the postsynaptic receptors, because it reduces the amplitude of both miniature IPSCs and the responses of excised patches to applied GABA. Thus, in the hippocampus, parallel inhibitory circuits are composed of separate populations of interneurons that contact anatomically segregated and pharmacologically distinct postsynaptic receptors.
尽管在CA1锥体神经元中已观察到两种动力学上不同的诱发GABAA反应（GABAA快速反应和GABAA缓慢反应），但对这些神经元中自发抑制性突触后电流（sIPSCs）的研究仅报道了一类事件，其上升和衰减动力学类似于GABAA快速反应。缺乏缓慢的sIPSCs使得GABAA缓慢反应的突触基础受到质疑。我们在此提供证据表明，这两种诱发反应均源于突触，因为存在两类最小诱发的、自发的和微小的IPSCs，它们分别对应于GABAA快速反应和GABAA缓慢反应。缓慢的sIPSCs很少出现，这表明产生这些事件的细胞自发放电率较低，这与产生快速sIPSCs的细胞不同。与诱发的GABAA快速反应和GABAA缓慢反应一样，快速和缓慢的sIPSCs受到呋塞米（一种亚型特异性GABAA拮抗剂）的不同调节。呋塞米通过直接作用于突触后受体来阻断快速IPSCs，因为它降低了微小IPSCs的幅度以及切除的膜片对施加的GABA的反应。因此，在海马体中，平行抑制性回路由不同的中间神经元群体组成，这些中间神经元与解剖学上分离且药理学上不同的突触后受体相接触。
