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首页> 外文期刊>Journal of Neurophysiology >Distinct GABAB actions via synaptic and extrasynaptic receptors in rat hippocampus in vitro.
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Distinct GABAB actions via synaptic and extrasynaptic receptors in rat hippocampus in vitro.

机译：体外大鼠海马中通过突触和突触外受体的不同GABA B作用。

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摘要

Intracellular recordings were obtained from pyramidal cells to examine gamma-aminobutyric acid-B (GABAB)-mediated synaptic mechanisms in the CA1 region of rat hippocampal slices. To investigate if heterogeneous ionic mechanisms linked to GABAB receptors originate from distinct sets of inhibitory fibers, GABAB-mediated monosynaptic late inhibitory postsynaptic potentials (IPSPs) were elicited in the presence of antagonists of ionotropic glutamate and GABAA receptors and of an inhibitor of GABA uptake and were compared after direct stimulation of inhibitory fibers in three different CA1 layers: stratum oriens, radiatum, and lacunosum-moleculare. No significant differences were found in mean amplitude, rise time, or time to decay to half-amplitude of IPSPs evoked from the three layers. Mean equilibrium potential (Erev) of late IPSPs was similar for all groups and close to the equilibrium potential of K+. Bath application of the GABAB antagonist CGP55845A blocked all monosynaptic late IPSPs. During recordings with micropipettes containing guanosine-5'-O-(3-thiotriphosphate) (GTPgammaS), the mean amplitude of all GABAB IPSPs gradually was reduced. Bath application of Ba2+ completely eliminated monosynaptic late IPSPs evoked from any of the stimulation sites. Late IPSPs were blocked completely during Ba2+ applications that reduced the GABAB-mediated hyperpolarizations elicited by local application of exogenous GABA only by approximately 50%. These results indicate that heterogenous K+ conductances activated by GABAB receptors do not originate from separate sets of inhibitory fibers in these layers. To examine if synchronous release of GABA from a larger number of inhibitory fibers could activate heterogeneous GABAB mechanisms, giant GABAB IPSPs were induced by 4-aminopyridine (4-AP) in the presence of antagonists of ionotropic glutamate and GABAA receptors. The amplitude and time course 4-AP-induced late IPSPs were approximately double that of evoked monosynaptic late IPSPs, but their voltage sensitivity, Erev, and antagonism by the GABAB antagonist CGP55845A and intracellular GTPgammaS were similar. Ba2+ completely abolished 4-AP-induced late IPSPs, whereas responses elicited by exogenous GABA were only reduced by approximately 50% in the same cells. These results indicate that synchronous activation of large numbers of inhibitory fibers, as induced by 4-AP, may not activate heterogenous GABAB-mediated conductances. Similarly, Ba2+ almost completely blocked late inhibitory postsynaptic currents evoked by stimulus trains. Overall, our results show that exogenous GABA can activate heterogenous K+ conductances via GABAB receptors, but that GABA released synaptically, either by electrical stimulation or 4-AP application, can only activate K+ conductances homogeneously sensitive to Ba2+. Thus GABAB receptors located at synaptic and extrasynaptic sites on hippocampal pyramidal cells may be linked to distinct K+ conductances.
机译：从锥体细胞获得细胞内记录，以检查大鼠海马切片CA1区中的γ-氨基丁酸-B（GABAB）介导的突触机制。为了研究与GABA B受体相关的异质离子机制是否源自不同组的抑制性纤维，在存在离子型谷氨酸和GABA A受体拮抗剂以及GABA摄取和抑制作用的抑制剂的存在下，诱发了GABA B介导的单突触后期抑制突触后电位（IPSP）。在三个不同的CA1层中直接刺激抑制性纤维后，进行了比较：原始层，放射状层和片状分子。在三层中诱发的IPSP的平均幅度，上升时间或衰减到半振幅的时间方面没有发现显着差异。所有组后期IPSP的平均平衡电位（Erev）均相似，接近K +的平衡电位。 GABAB拮抗剂CGP55845A的沐浴应用可阻断所有单突触晚期IPSP。在使用含鸟苷5'-O-（3-硫代三磷酸）（GTPgammaS）的微量移液器进行录制期间，所有GABAB IPSP的平均振幅逐渐降低。浴中Ba2 +的施用完全消除了任何刺激部位引起的单突触后期IPSP。后期IPSPs在Ba2 +施用期间被完全阻断，这将外源GABA局部施用引起的GABAB介导的超极化减少了仅约50％。这些结果表明，由GABAB受体激活的异质K +电导不是来自这些层中抑制纤维的不同集合。为了检查从大量抑制性纤维中同步释放GABA是否可以激活异质GABAB机制，在离子型谷氨酸和GABAA受体拮抗剂的存在下，由4-氨基吡啶（4-AP）诱导了巨大的GABAB IPSP。 4-AP诱导的晚期IPSP的幅度和时程约为诱发的单突触晚期IPSP的两倍，但GABAB拮抗剂CGP55845A和细胞内GTPγS的电压敏感性，Erev和拮抗作用相似。 Ba2 +完全废除了4-AP诱导的晚期IPSP，而在相同细胞中外源性GABA引起的应答仅降低了约50％。这些结果表明，由4-AP诱导的大量抑制性纤维的同步激活可能不会激活异源GABA B介导的电导。同样，Ba2 +几乎完全阻断了刺激火车诱发的晚期抑制性突触后电流。总体而言，我们的结果表明，外源性GABA可以通过GABAB受体激活异质性K +电导，但是通过电刺激或4-AP施加突触释放的GABA只能激活对Ba2 +均一敏感的K +电导。因此，位于海马锥体细胞突触和突触外位的GABA B受体可能与不同的K +电导相关。

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