دورية أكاديمية
Interactions between the Astrocytic Volume-Regulated Anion Channel and Aquaporin 4 in Hyposmotic Regulation of Vasopressin Neuronal Activity in the Supraoptic Nucleus
| العنوان: | Interactions between the Astrocytic Volume-Regulated Anion Channel and Aquaporin 4 in Hyposmotic Regulation of Vasopressin Neuronal Activity in the Supraoptic Nucleus |
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| المؤلفون: | Yang Liu, Xiao-Ran Wang, Yun-Hao Jiang, Tong Li, Shuo Ling, Hong-Yang Wang, Jia-Wei Yu, Shu-Wei Jia, Xiao-Yu Liu, Chun-Mei Hou, Vladimir Parpura, Yu-Feng Wang |
| المصدر: | Cells, Vol 12, Iss 13, p 1723 (2023) |
| بيانات النشر: | MDPI AG, 2023. |
| سنة النشر: | 2023 |
| المجموعة: | LCC:Cytology |
| مصطلحات موضوعية: | aquaporin 4, glial fibrillary acidic protein, LRRC8A, volume-regulated anion channels, regulatory volume decrease, Cytology, QH573-671 |
| الوصف: | We assessed interactions between the astrocytic volume-regulated anion channel (VRAC) and aquaporin 4 (AQP4) in the supraoptic nucleus (SON). Acute SON slices and cultures of hypothalamic astrocytes prepared from rats received hyposmotic challenge (HOC) with/without VRAC or AQP4 blockers. In acute slices, HOC caused an early decrease with a late rebound in the neuronal firing rate of vasopressin neurons, which required activity of astrocytic AQP4 and VRAC. HOC also caused a persistent decrease in the excitatory postsynaptic current frequency, supported by VRAC and AQP4 activity in early HOC; late HOC required only VRAC activity. These events were associated with the dynamics of glial fibrillary acidic protein (GFAP) filaments, the late retraction of which was mediated by VRAC activity; this activity also mediated an HOC-evoked early increase in AQP4 expression and late subside in GFAP-AQP4 colocalization. AQP4 activity supported an early HOC-evoked increase in VRAC levels and its colocalization with GFAP. In cultured astrocytes, late HOC augmented VRAC currents, the activation of which depended on AQP4 pre-HOC/HOC activity. HOC caused an early increase in VRAC expression followed by a late rebound, requiring AQP4 and VRAC, or only AQP4 activity, respectively. Astrocytic swelling in early HOC depended on AQP4 activity, and so did the early extension of GFAP filaments. VRAC and AQP4 activity supported late regulatory volume decrease, the retraction of GFAP filaments, and subside in GFAP-VRAC colocalization. Taken together, astrocytic morphological plasticity relies on the coordinated activities of VRAC and AQP4, which are mutually regulated in the astrocytic mediation of HOC-evoked modulation of vasopressin neuronal activity. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 2073-4409 84324821 |
| Relation: | https://www.mdpi.com/2073-4409/12/13/1723; https://doaj.org/toc/2073-4409 |
| DOI: | 10.3390/cells12131723 |
| URL الوصول: | https://doaj.org/article/ddbbb8f28ce843248214a1a6ad7fc3bc |
| رقم الأكسشن: | edsdoj.bbb8f28ce843248214a1a6ad7fc3bc |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 20734409 84324821 |
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| DOI: | 10.3390/cells12131723 |