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The perforant path projection to hippocampal area CA1 in the rat hippocampal-entorhinal cortex combined slice.

机译:大鼠海马-肠皮质复合切片中海马区CA1的穿孔路径投影。

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摘要

1. The perforant path projection from layer III of the entorhinal cortex to CA1 of the hippocampus was studied within a hippocampal-entorhinal combined slice preparation. We prevented contamination from the other main hippocampal pathways by removal of CA3 and the dentate gyrus. 2. Initially the projection was mapped using field potential recordings that suggested an excitatory sink in stratum lacunosum moleculare with an associated source in stratum pyramidale. 3. However, recording intracellularly from CA1 cells, stimulation of the perforant path produced prominent fast GABAA and slow GABAB IPSPs often preceded by small EPSPs. In a small number of cells we observed EPSPs only. 4. CNQX blocked excitatory and inhibitory responses. This indicated the presence of an intervening excitatory synapse between the inhibitory interneurone and the pyramidal cell. 5. Focal bicuculline applications revealed that the major site of GABAA inhibitory input was to stratum radiatum of CA1. 6. The inhibition activated by the perforant path was very effective at reducing simultaneously activated Schaffer collateral mediated EPSPs and suprathreshold-stimulated action potentials. 7. Blockade of fast inhibition increased excitability and enhanced slow inhibition. Both increases relied upon the activation of NMDA receptors. 8. Perforant path inputs activated prominent and effective disynaptic inhibition of CA1 cells. This has significance for the output of hippocampal processing during normal behaviour and also under pathological conditions.
机译:1.在海马-肠胃联合切片制备方法中,研究了从内嗅皮层III到海马CA1的穿孔路径投影。通过去除CA3和齿状回,我们防止了来自其他主要海马途径的污染。 2.最初,使用场电势记录对投影进行了映射,该记录暗示了黑胶质层分子中的兴奋性沉陷以及金字塔状层中的相关来源。 3.然而,通过从CA1细胞进行细胞内记录,对穿孔路径的刺激产生了明显的快速GABAA和缓慢的GABAB IPSP,通常在小EPSP之前。在少数细胞中,我们仅观察到EPSP。 4. CNQX阻断了兴奋性和抑制性反应。这表明抑制性中间神经元和锥体细胞之间存在介入性兴奋性突触。 5.局部双小分子的应用表明,GABAA抑制性输入的主要部位是CA1的放射状层。 6.穿孔途径激活的抑制作用在减少同时激活的沙弗尔侧支介导的EPSP和阈上刺激的动作电位方面非常有效。 7.快速抑制的阻断增加了兴奋性并增强了慢抑制。两种增加都依赖于NMDA受体的激活。 8.穿孔路径输入激活了对CA1细胞的显着和有效的突触抑制。这对于正常行为期间以及病理条件下的海马加工输出具有重要意义。

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