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视觉活动增强丘脑中继神经元的神经元兴奋性。

Visual activity enhances neuronal excitability in thalamic relay neurons.

作者信息

Duménieu Maël, Fronzaroli-Molinieres Laure, Naudin Loïs, Iborra-Bonnaure Cécile, Wakade Anushka, Zanin Emilie, Aziz Aurore, Ankri Norbert, Incontro Salvatore, Denis Danièle, Marquèze-Pouey Béatrice, Brette Romain, Debanne Dominique, Russier Michaël

机构信息

Aix-Marseille Université, INSERM, UNIS, Marseille, France.

Sorbonne Université, INSERM, CNRS, Institut de la Vision, Paris, France.

出版信息

Sci Adv. 2025 Jan 24;11(4):eadp4627. doi: 10.1126/sciadv.adp4627. Epub 2025 Jan 22.

DOI:10.1126/sciadv.adp4627
PMID:39841847
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11753433/
Abstract

Amblyopia, a highly prevalent loss of visual acuity, is classically thought to result from cortical plasticity. The dorsal lateral geniculate nucleus (dLGN) has long been held to act as a passive relay for visual information, but recent findings suggest a largely underestimated functional plasticity in the dLGN. However, the cellular mechanisms supporting this plasticity have not yet been explored. We show here that monocular deprivation (MD), an experimental model of amblyopia, reduces the intrinsic excitability of dLGN cells. Furthermore, dLGN neurons exhibit long-term potentiation of their intrinsic excitability (LTP-IE) when suprathreshold afferent retinal inputs are stimulated at 40 hertz or when spikes are induced with current injection. LTP-IE is observed after eye opening, requires calcium influx, is expressed through the down-regulation of Kv1 channels, and is altered following MD. In conclusion, our study provides the first evidence for intrinsic plasticity in dLGN neurons induced by natural stimuli.

摘要

弱视是一种极为常见的视力丧失，传统上认为它是由皮质可塑性导致的。长期以来，人们一直认为背侧外侧膝状核（dLGN）仅作为视觉信息的被动中继站，但最近的研究结果表明，dLGN的功能可塑性在很大程度上被低估了。然而，支持这种可塑性的细胞机制尚未得到探索。我们在此表明，单眼剥夺（MD）作为弱视的一种实验模型，会降低dLGN细胞的内在兴奋性。此外，当以40赫兹的频率刺激阈上视网膜传入输入或通过电流注入诱导动作电位时，dLGN神经元会表现出其内在兴奋性的长期增强（LTP-IE）。LTP-IE在睁眼后被观察到，需要钙内流，通过Kv1通道的下调来表达，并且在MD后会发生改变。总之，我们的研究为自然刺激诱导的dLGN神经元内在可塑性提供了首个证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58a4/11753433/b06eb157bdbd/sciadv.adp4627-f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58a4/11753433/b06eb157bdbd/sciadv.adp4627-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58a4/11753433/695cbd1b5f23/sciadv.adp4627-f1.jpg
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