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Reverberation of chloride-dependent synaptic potentials in the rat entorhinal cortex in vitro.

机译:在大鼠内嗅皮层中氯化物依赖性突触电位的回响。

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摘要

The spontaneous activity generated by rat entorhinal neurons during application of 4-aminopyridine (4AP; 50 microM) was studied with intracellular and extracellular field-potential recordings in an vitro slice preparation. Long-lasting depolarizations (LLDs) with amplitudes of 15 +/- 7.6 mV (mean +/- SD; n = 14) and durations of 1.65 +/- 0.77 s (n = 14) occurred at 0.036 +/- 0.01/s (n = 14). Each LLD was followed by a rhythmic sequence of depolarizing potentials (up to 22 events) with amplitudes of 4-30 mV, durations of 40-500 ms and frequency of 0.9 +/- 0.2/s (n = 14). These intracellular potentials were mirrored by negative-going field potentials, suggesting that they represented synchronous events. Membrane input resistance decreased by 79-86% during both LLDs and subsequent rhythmic depolarizations. Intracellular injection of steady depolarizing or hyperpolarizing current modified the amplitude of these potentials in a similar manner: the reversal potential of the LLDs and of the rhythmic depolarizations was -66.4 +/- 4 mV and -67.9 +/- 3.2 mV, respectively (n = 7). Intracellular injection of Cl- increased the amplitude of both types of potentials. Spontaneous LLDs continued to occur during application of the non-N-methyl-D-aspartate (NMDA) receptor antagonist 6-cyano-7-nitro-quinoxaline-2,3-dione (10 microM), a procedure that abolished the subsequent rhythmic depolarizations (n = 3). LLDs were blocked by further addition of the gamma-aminobutyric acid (GABA)A receptor antagonist bicuculline methiodide (10 microM, n = 3). Our findings demonstrate that during 4AP application entorhinal neurons generate glutamatergic-independent LLDs as well as synchronous, Cl(-)-dependent depolarizations that reverberate through non-NMDA-mediated excitatory circuits.
机译:在体外切片制备中,通过细胞内和细胞外场电位记录研究了在应用4-氨基吡啶(4AP; 50 microM)期间大鼠内脏神经元产生的自发活性。振幅为15 +/- 7.6 mV(平均值+/- SD; n = 14),持续时间为1.65 +/- 0.77 s(n = 14)的长效去极化(LLD)发生在0.036 +/- 0.01 / s (n = 14)。每个LLD后面都有一个去极化电位的节奏序列(最多22个事件),振幅为4-30 mV,持续时间为40-500 ms,频率为0.9 +/- 0.2 / s(n = 14)。这些细胞内电势被负向电场势所反映,表明它们代表同步事件。在LLD和随后的节律去极化过程中,膜的输入电阻均降低了79-86%。细胞内注入稳定的去极化或超极化电流以类似的方式改变了这些电位的幅度:LLD和有节奏的去极化的反向电位分别为-66.4 +/- 4 mV和-67.9 +/- 3.2 mV(n = 7)。胞内注射Cl-增加了两种电位的幅度。在使用非N-甲基-D-天冬氨酸(NMDA)受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮(10 microM)的过程中,自发性LLD继续发生,这一过程取消了随后的节律性去极化(n = 3)。通过进一步添加γ-氨基丁酸(GABA)A受体拮抗剂双小分子甲硫氨酸(10 microM,n = 3)来阻断LLD。我们的发现表明,在4AP应用过程中,内嗅神经元会生成非谷氨酸能依赖性LLD以及通过非NMDA介导的兴奋性回路回荡的同步,依赖Cl(-)的去极化。

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