GABAA currents in immature dentate gyrus granule cells.
GABAA currents in immature dentate gyrus granule cells.
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未成熟齿状回颗粒细胞中的 GABAA 电流。
DOI：
10.1152/jn.1998.80.5.2255
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Trommer,BL
中科院分区：
文献类型：
--
作者：
Liu,YB;Ye,GL;Liu,XS;Pasternak,JF;Trommer,BL
刘应兵，叶桂兰，刘雪松，Joseph F. Pasternak和Barbara L. Trommer.未成熟齿状回颗粒细胞中的GABA电流.神经生理学杂志80：2255-2267，1998.采用全细胞膜片钳和短杆菌肽穿孔膜片钳技术，研究幼年大鼠海马齿状回颗粒细胞γ-氨基丁酸（GABA）电流。GC在出生后和异步地产生，使得它们可以在第一个月内在DG中成熟的不同阶段被检测到。相比之下，抑制性中间神经元是在胚胎中产生的，即使它们的目标GC和GC兴奋性连接仍在形成，它们的电路也发育良好。在这项研究中，两个GABA电流诱发的GC由内侧穿通路刺激进行了比较。第一个是通过谷氨酸受体阻断分离的GABA中间神经元，是GABA中间神经元直接激活的产物，其单突触输入到记录的GC（单突触GABAA）。单突触GABA A的电流-电压关系显示轻微的外向整流，10 μM荷包牡丹碱可消除97%，与GC突触后电流的兴奋成分在时间上一致，如其他脑区GABA A电流所述。第二种是一种新的GABA反应，可在10 μM荷包牡丹碱中检测到，仅在GC成熟的最早阶段存在于GC上。与单突触GABAA不同，这种短暂的GABA通过谷氨酸受体阻断剂消除，因此可能是由通过介入的谷氨酸能突触（多突触）激活的中间神经元产生的。它主要是氯化物介导的，具有26%的相对碳酸氢盐/氯化物渗透率比，并通过浴应用萨氯芬和士的宁或细胞内钙螯合作用不变。100 μM印防己毒素可拮抗97%，100 μM荷包牡丹碱可拮抗99%。因此，该电流是相对荷包牡丹碱（BMI）抗性的GABAA电流（BMIR-GABAA）。与单突触GABAA相比，BMIR-GABAA具有较晚的峰值，较缓慢的衰减过程，以及明显的外向整流。无论是在全细胞中记录还是用短杆菌肽穿孔片记录以保持天然内部氯浓度，其逆转电位为7-8 mV去极化至单突触GABA A的电位。总之，这些数据可能表明，BMIR-GABAA是诱发的解剖隔离群体的中间神经元激活一个独特的，发育调节GABAA受体。此外，该电流的瞬态性质加上其时间特性，排除与突触反应的兴奋性成分的重叠，与营养或信号传导而不是主要抑制的作用一致。
Liu, Ying Bing, Gui-Lan Ye, Xue-Song Liu, Joseph F. Pasternak, and Barbara L. Trommer.GABAACurrents in immature dentate gyrus granule cells.J. Neurophysiol.80: 2255–2267, 1998. We used whole cell patch clamp and gramicidin perforated patch recordings in hippocampal slices to study γ-aminobutyric acid (GABA) currents in granule cells (GCs) from juvenile rat dentate gyrus (DG). GCs are generated postnatally and asynchronously such that they can be detected at different stages of their maturation in DG within the first month. In contrast, inhibitory interneurons are generated embryonically, and their circuitry is well developed even as their target GCs and GC excitatory connections are still being formed. In this study, two GABA currents evoked in GCs by medial perforant path stimulation are compared. The first, pharmacologically isolated by glutamate receptor blockade, is the product of direct activation of GABA interneurons with monosynaptic input to the recorded GC (monosynaptic GABAA). Monosynaptic GABAAdisplays slight outward rectification of its current-voltage relation, is 97% eliminated by 10 μM bicuculline and coincides temporally with the excitatory components of GC postsynaptic currents as has been described for GABAAcurrents in other brain regions. The second is a novel GABA response that is detectable in 10 μM bicuculline and is present on GCs only at the earliest stages of their maturation. Unlike monosynaptic GABAA, this transient GABA is eliminated by glutamate receptor blockade and hence is likely to be generated by interneurons activated via an intervening glutamatergic synapse (polysynaptically). It is predominantly chloride mediated, has a relative bicarbonate/chloride permeability ratio of 26%, and is unchanged by bath-applied saclofen and strychnine or by intracellular calcium chelation. It is 97% antagonized by 100 μM picrotoxin and 99% antagonized by 100 μM bicuculline. This current is thus a relatively bicuculline (BMI)-resistant GABAAcurrent (BMIR-GABAA). Compared with monosynaptic GABAA, BMIR-GABAAhas a later peak, slower time course of decay, and marked outward rectification. Its reversal potential is 7–8 mV depolarized to that of monosynaptic GABAAwhether recorded in whole cell or with gramicidin perforated patch to preserve native internal chloride concentration. Together these data may suggest that BMIR-GABAAis evoked by an anatomically segregated population of interneurons activating a unique, developmentally regulated GABAAreceptor. Further, the transient nature of this current coupled with its temporal characteristics that preclude overlap with the excitatory components of the synaptic response are consistent with a role that is trophic or signaling rather than primarily inhibitory.
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