Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS, Saint Petersburg 194223, Russia.
Ioffe Institute, Saint Petersburg 194021, Russia.
Int J Mol Sci. 2024 Jul 10;25(14):7568. doi: 10.3390/ijms25147568.
Epilepsy is known to cause alterations in neural networks. However, many details of these changes remain poorly understood. The objective of this study was to investigate changes in the properties of hippocampal CA1 pyramidal neurons and their synaptic inputs in a rat lithium-pilocarpine model of epilepsy. In the chronic phase of the model, we found a marked loss of pyramidal neurons in the CA1 area. However, the membrane properties of the neurons remained essentially unaltered. The results of the electrophysiological and morphological studies indicate that the direct pathway from the entorhinal cortex to CA1 neurons is reinforced in epileptic animals, whereas the inputs to them from CA3 are either unaltered or even diminished. In particular, the dendritic spine density in the , where the direct pathway from the entorhinal cortex terminates, was found to be 2.5 times higher in epileptic rats than in control rats. Furthermore, the summation of responses upon stimulation of the temporoammonic pathway was enhanced by approximately twofold in epileptic rats. This enhancement is believed to be a significant contributing factor to the heightened epileptic activity observed in the entorhinal cortex of epileptic rats using an ex vivo 4-aminopyridine model.
癫痫被认为会导致神经网络的改变。然而，这些变化的许多细节仍未被很好地理解。本研究的目的是调查锂-匹罗卡品癫痫大鼠模型中海马 CA1 锥体神经元及其突触输入的特性变化。在模型的慢性期，我们发现 CA1 区域的锥体神经元明显丢失。然而，神经元的膜特性基本没有改变。电生理和形态学研究的结果表明，在癫痫动物中，从内侧嗅皮层到 CA1 神经元的直接通路得到了加强，而来自 CA3 的输入则不变或甚至减少。特别是，在 ，即内侧嗅皮层到 CA1 神经元的直接通路终止的部位，棘突密度在癫痫大鼠中比在对照组大鼠中高 2.5 倍。此外，癫痫大鼠中刺激颞极弓状束时的反应总和增强了约两倍。这种增强被认为是在使用 4-氨基吡啶体外模型时观察到癫痫大鼠内侧嗅皮层中癫痫活动增加的一个重要因素。
