Abstract—We analyzed possible mechanisms of the influence of the supramammillary nucleus of the hypothalamus (SMN) on the activity of granule cells of the dentate gyrus and pyramidal neurons of the CA2 field of the hippocampus. We used known data on the functional organization of excitatory and inhibitory interactions in the neural network, which includes the SMN, hippocampus, septum, and entorhinal cortex. We propose that the induction of long-term potentiation in the perforant path inputs to granule cells and pyramidal neurons of the CA2 field during simultaneous stimulation of the SMN and the entorhinal cortex is promoted by disinhibition, which involves interconnected inhibitory neurons located in different fields of the hippocampus, the septum, and the SMN. In the waking state, the glutamatergic input from the SMN to the CA2 field promotes the potentiation of inputs from the entorhinal cortex and from the CA3 field to the pyramidal neurons of the CA2 field, which facilitates the propagation of signals through the trisynaptic hippocampal pathway. Taking into account the known data on the increased activity of the SMN during paradoxical sleep, data on the participation of the SMN in an increase in the activity of granule cells and pyramidal neurons of the CA2 field, and data on the high efficiency of input from the CA2 field into the CA1 field, we hypothesized that during paradoxical sleep, when the transmission of information through the classical trisynaptic pathway is suppressed, it is transferred to the CA1 field through the dentate gyrus and CA2 field. Our analysis suggests that the SMN-induced facilitation of signal transmission through different hippocampal fields as well as an increase in the activity of SMN and granule cells during paradoxical sleep, which promotes neurogenesis, may underlie the participation of SMN in memory processes.

摘要-我们分析了下丘脑上乳状核（SMN）对齿状回的颗粒细胞和海马CA2区域的锥体神经元活性的影响的可能机制。我们使用了有关神经网络中兴奋性和抑制性相互作用的功能组织的已知数据，其中包括SMN，海马，隔膜和内嗅皮层。我们建议，在同时刺激SMN和内嗅皮层的过程中，通向CA2区域的颗粒细胞和锥体神经元的穿孔路径输入中的长时程增强诱导通过去抑制作用来促进，这涉及位于不同领域的相互连接的抑制性神经元。海马，隔膜和SMN。在清醒状态下 从SMN到CA2场的谷氨酸能输入促进了从内嗅皮层以及从CA3场到CA2场的锥体神经元的输入增强，这促进了信号通过三突触海马通路的传播。考虑到有关悖论性睡眠期间SMN活动增加的已知数据，有关SMN参与CA2场的颗粒细胞和锥体神经元活动增加的数据以及有关来自S2的高输入效率的数据从CA2场到CA1场，我们假设在自相矛盾的睡眠中，当信息通过经典三突触途径的传递受到抑制时，它将通过齿状回和CA2场转移到CA1场。