Recruitment nf GABAergic inhibition and synchronization of inhibitory interneurons in rat neocortex

Recruitment nf GABAergic inhibition and synchronization of inhibitory interneurons in rat neocortex
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DOI:
10.1152/jn.1997.77.6.3134
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发表时间:
1997-06-01
影响因子:
2.5
通讯作者:
Benardo, LS
Benardo, LS
中科院分区:
医学3区
文献类型:
--
作者:
Benardo, LS

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从大鼠新皮层切片中的锥体细胞和中间神经元细胞获得细胞内记录,以检查GABA能抑制和抑制性中间神经元的募集。在致惊剂4-氨基吡啶(4-AP)存在下,兴奋性氨基酸(EAA)离子传递被阻断后,锥体神经元有节律地(每10-40 s)同步出现大幅度三相抑制性突触后电位(IPSPs)。在暴露于γ-氨基丁酸-A(GABA(A))受体拮抗剂印防己毒素后,这些细胞中持续存在大幅度的单相慢IPSP。在4-AP和EAA阻断剂的存在下,中间神经元表现出周期性的尖峰放电。虽然一些尖峰骑在一个潜在的突触去极化,许多有节奏的发射包括尖峰具有高度可变的幅度,突然从基线,即使在超极化。尽管中间神经元中的单相慢IPSPs持续存在,但印防己毒素暴露完全抑制了尖峰放电和去极化突触电位。这表明,该中间神经元映射子集参与产生快GABA(A)IPSP,但不参与产生慢GABA(B)IPSP。通过细胞内注射神经生物素或荧光染料荧光黄CH来确认细胞形态。向中间神经元中注射染料通常(>70%)导致2至6个细胞的标记(染料偶联)。这些结果表明,GABA(A)能神经元可能通过突触激活的GABA(A)受体的去极化作用和涉及电紧张耦合的机制,通过反复侧支同步化。虽然抑制性神经元介导GABA(B)IPSP可能被兴奋性GABA(A)机制所携带,但它们似乎是能够独立地与自主起搏起作用的GABA能神经元的单独子集。
Intracellular recordings were obtained from pyramidal and interneuronal cells in rat neocortical slices to examine the recruitment of GABAergic inhibition and inhibitory interneurons. In the presence of the convulsant agent 4-aminopyridine (4-AP), after excitatory amino acid (EAA) ionotropic transmission was blocked, large-amplitude triphasic inhibitory postsynaptic potentials (IPSPs) occurred rhythmically (every 10-40 s) and synchronously in pyramidal neurons. After exposure to the gamma-aminobutyric acid-A (GABA(A)) receptor antagonist picrotoxin, large-amplitude monophasic slow IPSPs persisted in these, cells. In the presence of 4-AP and EAA blockers, interneurons showed periodic spike firing. Although some spikes rode on an underlying synaptic depolarization, much of the rhythmic firing consisted of spikes having highly variable amplitudes, arising abruptly from baseline, even during hyperpolarization. The spike firing and depolarizing synaptic potentials were completely suppressed by picrotoxin exposure, although monophasic slow IPSPs persisted in interneurons. This suggests that this subset of interneurons map participate in generating fast GABA(A) IPSPs, but not slow GABA(B) IPSPs. Cell morphology was confirmed by intracellular injection of neurobiotin or the fluorescent dye Lucifer yellow CH. Dye Injection into interneurons often (>70%) resulted ill the labeling of two to six cells (dye coupling. These findings suggest that GABA(A)ergic neurons may be synchronized via recurrent collaterals through the depolarizing action of synaptically activated GABA(A) receptors and a mechanism involving electrotonic coupling. Although inhibitory neurons mediating GABA(B) IPSPs may be entrained by the excitatory GABA(A) mechanism, they appear to be a separate subset of GABAergic neurons capable of functioning independently with autonomous pacing.