Abstract

Purpose/aim

The role of cholinergic neurotransmission in the hippocampus remains controversial since different studies showed either no influence or its modulatory effect on glutamatergic hippocampal synapses. It remains unclear whether septal cholinergic input can modulate plasticity of synapses formed by CA3 pyramids on CA1 neurons. The aim of the study was to clarify the role of septal input in the development of LTP in this synapse.

Materials and methods

We recorded in vivo in rats under urethane anesthesia focal excitatory postsynaptic potential (fEPSP) characteristics in CA1 area after stimulation of the ventral hippocampal commissure (VHC), which contains both CA3 axons innervating CA1 neurons and cholinergic axons coming from the medial septum. We performed two series of experiments in which LTP was induced by tetanization of either VHC or medial septal area (MSA). Degeneration of cholinergic neurons in MSA was induced by intraseptal injection of 192IgG-saporin.

Results

In both experimental series, tetanization induced an increase in fEPSP amplitude which lasted for at least 40 min after tetanic stimulation, although tetanization of VHC induced a larger increase in fEPSP amplitude compared to MSA tetanization. Elimination of septal cholinergic neurons by 192IgG-saporin abolished LTP development in both experimental series. This suppression of LTP in animals with cholinergic deficit was not due to loss of hippocampal neurons.

Conclusions

Our data suggest that activation of septal cholinergic fibers during tetanization is a critical factor of LTP induction in the hippocampal CA3 to CA1 synapses.

中文翻译：

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海马 CA3 到 CA1 突触的长期增强可能在体内通过激活间隔胆碱能输入来诱导

摘要

目的/目标

胆碱能神经传递在海马中的作用仍然存在争议，因为不同的研究表明它对谷氨酸能海马突触没有影响或有调节作用。目前尚不清楚间隔胆碱能输入是否可以调节 CA1 神经元上 CA3 金字塔形成的突触的可塑性。该研究的目的是阐明间隔输入在该突触中 LTP 发展中的作用。

材料和方法

我们在腹侧海马连合 (VHC) 刺激后，在氨基甲酸乙酯麻醉下的大鼠体内记录了 CA1 区域的局灶性兴奋性突触后电位 (fEPSP) 特征，其中包含支配 CA1 神经元的 CA3 轴突和来自内侧隔膜的胆碱能轴突。我们进行了两个系列的实验，其中 LTP 是由 VHC 或内侧间隔区 (MSA) 的强直化诱导的。MSA 中胆碱能神经元的变性是通过间隔内注射 192IgG-皂草素诱导的。

结果

在这两个实验系列中，强直化导致 fEPSP 幅度增加，在强直刺激后持续至少 40 分钟，尽管与 MSA 强直化相比，VHC 的强直化导致 fEPSP 幅度的增加更大。192IgG-皂草素消除间隔胆碱能神经元消除了两个实验系列中的 LTP 发展。这种对胆碱能缺陷动物 LTP 的抑制不是由于海马神经元的损失。

结论

我们的数据表明，在强直化过程中间隔胆碱能纤维的激活是海马 CA3 到 CA1 突触中 LTP 诱导的关键因素。