Illanes-González Javiera, Flores-Muñoz Carolina, Vitureira Nathalia, Ardiles Álvaro O
Centro Interdisciplinario de Neurociencia de Valparaíso, Facultad de Ciencias, Universidad de Valparaíso, Valparaíso 2360102, Chile; Centro para la Investigación Traslacional en Neurofarmacología, CItNe, Universidad de Valparaíso, Valparaíso, Chile.
Unidad Académica de Fisiología, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay.
Neurosci Biobehav Rev. 2025 Jul;174:106173. doi: 10.1016/j.neubiorev.2025.106173. Epub 2025 Apr 22.
The Pannexin 1 channel is a membrane protein widely expressed in various vertebrate cell types, including microglia, astrocytes, and neurons within the central nervous system. Growing research has demonstrated the significant involvement of Panx1 in synaptic physiology, such as its contribution to long-term synaptic plasticity, with a particular focus on the hippocampus, an essential structure for learning and memory. Investigations studying the role of Panx1 in synaptic plasticity have utilized knockout animal models and channel inhibition techniques, revealing that the absence or blockade of Panx1 channels in this region promotes synaptic potentiation, dendritic arborization, and spine formation. Despite substantial progress, the precise mechanism by which Panx1 regulates synaptic plasticity remains to be determined. Nevertheless, evidence suggests that Panx1 may exert its influence by releasing signaling molecules, such as adenosine triphosphate (ATP), or through the clearance of endocannabinoids (eCBs). This review aims to comprehensively explore the current literature on the role of Panx1 in synapses. By examining relevant articles, we seek to enhance our understanding of Panx1's contribution to synaptic fundamental processes and the potential implications for cognitive function.
泛连接蛋白1通道是一种膜蛋白,广泛表达于各种脊椎动物细胞类型中,包括中枢神经系统中的小胶质细胞、星形胶质细胞和神经元。越来越多的研究表明,泛连接蛋白1在突触生理学中发挥着重要作用,例如其对长期突触可塑性的贡献,尤其聚焦于海马体,这是学习和记忆的重要结构。研究泛连接蛋白1在突触可塑性中作用的调查利用了基因敲除动物模型和通道抑制技术,结果显示该区域泛连接蛋白1通道的缺失或阻断会促进突触增强、树突分支和棘突形成。尽管取得了重大进展,但泛连接蛋白1调节突触可塑性的精确机制仍有待确定。然而,有证据表明,泛连接蛋白1可能通过释放信号分子(如三磷酸腺苷(ATP))或通过清除内源性大麻素(eCBs)来发挥其影响。本综述旨在全面探讨当前关于泛连接蛋白1在突触中作用的文献。通过研究相关文章,我们试图加深对泛连接蛋白1对突触基本过程的贡献以及对认知功能潜在影响的理解。