---
title: "ESCRT-I Inhibition Restores NMDAR Function and Synaptic Homeostasis in a Cellular Schizophrenia Mo"
id: "biorxiv-12-escrt-i-inhibition-protects-against-nmdar-hypofunction-and-restores-synaptic"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-12-escrt-i-inhibition-protects-against-nmdar-hypofunction-and-restores-synaptic"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.09.07.749795v1?rss=1"
published_at: "2026-09-13T07:45:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# ESCRT-I Inhibition Restores NMDAR Function and Synaptic Homeostasis in a Cellular Schizophrenia Mo
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-12-escrt-i-inhibition-protects-against-nmdar-hypofunction-and-restores-synaptic
- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.09.07.749795v1?rss=1)
- **Published At:** 2026-09-13T07:45:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- N-methyl-D-aspartate receptor (**NMDAR**) hypofunction is implicated as a core pathophysiological mechanism in schizophrenia, but direct potentiation of NMDARs has had limited clinical success, possibly because receptor trafficking and surface stability are not addressed. - The endosomal sorting complexes required for transport (**ESCRT**) machinery directs lysosomal sorting of internalised membrane proteins; its role in synaptic receptor homeostasis during glutamatergic dysfunction was previously unclear. - Phencyclidine (**PCP**) — a non-competitive NMDAR antagonist — was used to create a cellular model of persistent NMDAR hypofunction and schizophrenia-like phenotypes in primary hippocampal neurons. - Sub-chronic PCP exposure induced persistent **NMDAR hypofunction**, impaired GABAergic transmission, and collapse of **excitation/inhibition (E/I) balance** in these neurons. - Genetic inhibition (knockdown) of the ESCRT-I component **TSG101** prevented PCP-induced deficits and allowed functional recovery after PCP washout. - TSG101 knockdown increased surface expression of functional **NMDARs** and **GABAA receptors** without changing receptor pharmacology or intrinsic biophysical properties. - At the network level, TSG101 knockdown restored inhibitory tone, normalised excitatory activity, and stabilised **E/I balance** in the cultured hippocampal networks. - TSG101 knockdown also rescued PCP-induced reductions in synaptic markers and signalling: PSD-95 and BDNF levels were restored, ERK1/2 signalling was re-established, and activity-dependent nuclear translocation of Fos-like (Fos-L) proteins returned, indicating recovery of transcriptional plasticity. - The findings identify **ESCRT-I** as a regulator of synaptic stability and suggest endosomal sorting pathways as a potential therapeutic target for schizophrenia. - The work is reported as a preprint and has not undergone peer review; competing interests note an author with a role in a biotechnology company, and all authors otherwise declared no conflicts related to the publication.
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Mohamed Shalaby 1 University of Bradford; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Mohamed%2BShalaby%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Shalaby%20M&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMohamed%2BShalaby%2B) Vincenzo Prato 2 University of Leeds * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Vincenzo%2BPrato%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Prato%20V&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AVincenzo%2BPrato%2B) * [ORCID record for Vincenzo Prato](http://orcid.org/0000-0002-1887-5556 "Open in new tab") Jacobo Gomez Elies 1 University of Bradford; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Jacobo%2BGomez%2BElies%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Elies%20JG&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJacobo%2BGomez%2BElies%2B) * [ORCID record for Jacobo Gomez Elies](http://orcid.org/0000-0002-2518-8412 "Open in new tab") Nikita Gamper 2 University of Leeds * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Nikita%2BGamper%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Gamper%20N&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ANikita%2BGamper%2B) * [ORCID record for Nikita Gamper](http://orcid.org/0000-0001-5806-0207 "Open in new tab") Samantha Louise Mclean 1 University of Bradford; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Samantha%2BLouise%2BMclean%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Mclean%20SL&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ASamantha%2BLouise%2BMclean%2B) * [ORCID record for Samantha Louise Mclean](http://orcid.org/0000-0001-9328-8928 "Open in new tab") Sriharsha Kantamneni 1 University of Bradford; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Sriharsha%2BKantamneni%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Kantamneni%20S&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ASriharsha%2BKantamneni%2B) * For correspondence: s.kantamneni@bradford.ac.uk * [Abstract](https://www.biorxiv.org/content/10.64898/2026.09.07.749795v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5777830/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.09.07.749795v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5777830/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.09.07.749795v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5777830/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.09.07.749795v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5777830/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract N-methyl-D-aspartate receptor (NMDAR) hypofunction is a central pathophysiological mechanism in schizophrenia, yet direct NMDAR potentiation has shown limited clinical benefit, potentially because it fails to address deficits in receptor trafficking and surface stability. The endosomal sorting complexes required for transport (ESCRT) machinery governs the lysosomal fate of internalised membrane proteins, but its role in synaptic receptor homeostasis during glutamatergic dysfunction remains unclear. Phencyclidine (PCP), a non-competitive NMDAR antagonist, is widely used to model NMDAR hypofunction and schizophrenia-like phenotypes. Here, we show that sub-chronic PCP exposure induced persistent NMDAR hypofunction, impaired GABAergic transmission, and collapsed of excitation/inhibition (E/I) balance in primary hippocampal neurons. Genetic inhibition of the ESCRT-I component TSG101 prevented these deficits, enabled functional recovery following PCP washout, and increased surface expression of functional NMDARs and GABAA receptors without altering receptor pharmacology or biophysical properties. At the network level, TSG101 knockdown restored inhibitory tone, normalised excitatory activity, and stabilised E/I balance. Moreover, TSG101 knockdown rescued PCP-induced reductions in PSD-95 and BDNF, restored ERK1/2 signalling, and re-established activity-dependent nuclear translocation of Fos-like (Fos-L), consistent with reactivation of transcriptional plasticity. These findings identify ESCRT-I as a regulator of synaptic stability, positioning endosomal sorting pathways as a potential therapeutic target for schizophrenia. ### Competing Interest Statement SK is a shareholder, founding director and CEO of Hado Therapeutics Limited (UK Registered: 12240559). All authors have no conflicts of interest or declarations in relation to this publication. 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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[ Download PDF](https://www.biorxiv.org/content/10.64898/2026.09.07.749795v1.full.pdf) Print/Save Options [Download PDF](https://www.biorxiv.org/content/biorxiv/early/2026/09/12/2026.09.07.749795.full.pdf)Full Text & In-line FiguresXML [More Info](https://www.biorxiv.org/about/FAQ#PrintOptions "More Information on Print/Save Options") [ Email](https://www.biorxiv.org/ "Email this Article") [ Share](https://www.biorxiv.org/) ESCRT-I Inhibition Protects against NMDAR Hypofunction and Restores Synaptic Homeostasis in a Cellular Model of Schizophrenia Mohamed Shalaby, Vincenzo Prato, Jacobo Gomez Elies, Nikita Gamper, Samantha Louise Mclean, Sriharsha Kantamneni bioRxiv 2026.09.07.749795; doi: https://doi.org/10.64898/2026.09.07.749795 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. 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