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下丘脑通过上丘脑对海马 CA1 中间神经元的调节。

Hypothalamic regulation of hippocampal CA1 interneurons by the supramammillary nucleus.

机构信息

Department of Neurosciences, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA.

Department of Neurosciences, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA.

出版信息

Cell Rep. 2024 Nov 26;43(11):114898. doi: 10.1016/j.celrep.2024.114898. Epub 2024 Oct 23.

DOI:10.1016/j.celrep.2024.114898
PMID:39446584
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11644823/
Abstract

The hypothalamic supramammillary nucleus (SuM) projects heavily to the hippocampus to regulate hippocampal activity and plasticity. Although the projections from the SuM to the dentate gyrus (DG) and CA2 have been extensively studied, whether the SuM projects to CA1, the main hippocampal output region, is unclear. Here, we report a glutamatergic pathway from the SuM that selectively excites CA1 interneurons in the border between the stratum radiatum (SR) and the stratum lacunosum-moleculare (SLM). We find that the SuM projects selectively to a narrow band in the CA1 SR/SLM and monosynaptically excites SR/SLM interneurons, including vasoactive intestinal peptide-expressing (VIP) and neuron-derived neurotrophic factor-expressing (NDNF) cells, but completely avoids making monosynaptic contacts with CA1 pyramidal neurons (PNs) or parvalbumin-expressing (PV) or somatostatin-expressing (SOM) cells. Moreover, SuM activation drives spikes in most SR/SLM interneurons to suppress CA1 PN excitability. Taken together, our findings reveal that the SuM can directly regulate hippocampal output region CA1, bypassing CA2, CA3, and the DG.

摘要

下丘脑穹窿上核（SuM）大量投射到海马体，以调节海马体的活动和可塑性。尽管 SuM 到齿状回（DG）和 CA2 的投射已经得到了广泛的研究，但 SuM 是否投射到海马体的主要输出区域 CA1 尚不清楚。在这里，我们报告了一条来自 SuM 的谷氨酸能通路，它选择性地兴奋 SR/SLM 交界处的 CA1 中间神经元。我们发现 SuM 选择性地投射到 CA1 SR/SLM 的一个狭窄带，并对 SR/SLM 中间神经元进行单突触兴奋，包括血管活性肠肽表达（VIP）和神经元衍生的神经营养因子表达（NDNF）细胞，但完全避免与 CA1 锥体神经元（PNs）或表达 Parvalbumin（PV）或 Somatostatin（SOM）的细胞进行单突触接触。此外，SuM 的激活驱动大多数 SR/SLM 中间神经元的尖峰，从而抑制 CA1 PN 的兴奋性。综上所述，我们的发现表明，SuM 可以直接调节海马体的输出区域 CA1，绕过 CA2、CA3 和 DG。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/e4f7baf4154c/nihms-2038871-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/56b9c8d95039/nihms-2038871-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/f3386727174d/nihms-2038871-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/18b81ae293c6/nihms-2038871-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/8626b9382ca3/nihms-2038871-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/6ae90cb78475/nihms-2038871-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/e4f7baf4154c/nihms-2038871-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/56b9c8d95039/nihms-2038871-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/f3386727174d/nihms-2038871-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/18b81ae293c6/nihms-2038871-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/8626b9382ca3/nihms-2038871-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/6ae90cb78475/nihms-2038871-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2248/11644823/e4f7baf4154c/nihms-2038871-f0007.jpg

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