---
title: "Volume-regulated anion channel (VRAC) dysfunction drives depression- and anxiety-like phenotypes i"
id: "biorxiv-7-altered-volume-regulated-anion-channel-activity-contributes-to-depression-and"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-7-altered-volume-regulated-anion-channel-activity-contributes-to-depression-and"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.07.22.740018v1?rss=1"
published_at: "2026-07-27T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Volume-regulated anion channel (VRAC) dysfunction drives depression- and anxiety-like phenotypes i
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-7-altered-volume-regulated-anion-channel-activity-contributes-to-depression-and
- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.07.22.740018v1?rss=1)
- **Published At:** 2026-07-27T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The study tested the role of the **volume-regulated anion channel (VRAC)** in affective disorder–related phenotypes using zebrafish as a model. - VRAC function was disrupted in two ways: pharmacological inhibition and morpholino-mediated knockdown of **lrrc8aa**, the zebrafish ortholog of mammalian **LRRC8A**, the essential VRAC subunit. - Loss or inhibition of VRAC produced **anxiety-like** and **depression-like** behaviours in zebrafish larvae and altered expression of genes previously associated with affective disorders. - Transcriptomic profiling of lrrc8aa-deficient larvae showed dysregulation of pathways linked to neuronal signalling and cellular stress responses. - Pharmacological activation of VRAC with **zinc pyrithione (ZPT)** improved behavioural abnormalities and partially normalized altered gene expression in larvae. - In adult zebrafish exposed to chronic unpredictable stress, ZPT produced **antidepressant- and anxiolytic-like** effects comparable to imipramine and normalized elevated **monoamine oxidase (mao)** expression. - Findings indicate that reduced VRAC activity contributes to both molecular and behavioural signatures relevant to depression and anxiety, suggesting VRAC as a potential therapeutic target for novel antidepressant development. - The work is a bioRxiv preprint from a group at the Indian Institute of Technology Madras and was funded in part by the Indian Council of Medical Research. The manuscript has not been peer reviewed.
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Amal Kanti Bera Indian Institute of Technology Madras * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Amal%2BKanti%2BBera%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Bera%20AK&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAmal%2BKanti%2BBera%2B) * [ORCID record for Amal Kanti Bera](http://orcid.org/0000-0003-0362-5578 "Open in new tab") * For correspondence: amal@iitm.ac.in Athira Ajith Indian Institute of Technology Madras * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Athira%2BAjith%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Ajith%20A&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAthira%2BAjith%2B) * [ORCID record for Athira Ajith](http://orcid.org/0009-0003-8902-0525 "Open in new tab") Durai Shalu Indian Institute of Technology Madras * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Durai%2BShalu%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Shalu%20D&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ADurai%2BShalu%2B) * [ORCID record for Durai Shalu](http://orcid.org/0009-0003-4145-157X "Open in new tab") Rudrakant Sharma Indian Institute of Technology Madras * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Rudrakant%2BSharma%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Sharma%20R&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ARudrakant%2BSharma%2B) * [ORCID record for Rudrakant Sharma](http://orcid.org/0009-0009-6253-9726 "Open in new tab") Gautam Mohapatra Indian Institute of Technology Madras * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Gautam%2BMohapatra%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Mohapatra%20G&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AGautam%2BMohapatra%2B) * [Abstract](https://www.biorxiv.org/content/10.64898/2026.07.22.740018v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5657457/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.07.22.740018v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5657457/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.07.22.740018v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5657457/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.07.22.740018v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5657457/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.07.22.740018v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5657457/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Major depressive disorder (MDD) is a leading cause of global morbidity and mortality. Unfortunately, a substantial proportion of patients do not respond adequately to currently available therapies, highlighting the need for new therapeutic targets. Here, we investigated the role of volume-regulated anion channel (VRAC) in depression-related phenotypes using zebrafish. Disruption of VRAC function, either by pharmacological inhibition or morpholino-mediated knockdown of lrrc8aa, the zebrafish ortholog of mammalian LRRC8A, the obligatory subunit required for VRAC function, induced anxiety- and depression-like behaviours in zebrafish larvae and altered the expression of genes associated with affective disorders. Transcriptomic analysis of lrrc8aa-deficient larvae revealed dysregulation of pathways involved in neuronal signalling and cellular stress responses. Conversely, pharmacological activation of VRAC with zinc pyrithione (ZPT) improved behavioural abnormalities and partially restored altered gene expression. In adult zebrafish subjected to chronic unpredictable stress, ZPT produced antidepressant- and anxiolytic-like effects comparable to those of imipramine and normalized elevated monoamine oxidase (mao) expression. Together, these findings indicate that reduced VRAC function contributes to depression- and anxiety-related behavioural and molecular phenotypes and identify VRAC as a potential target for the development of novel antidepressant therapies. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared Indian Council of Medical Research, 5/4-5/Ad-hoc/Neuro/206//2020-NCD-I Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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