ArticleCell reports2025
Loss of the proton-activated chloride channel in neurons impairs AMPA receptor endocytosis and LTD via endosomal hyper-acidification.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effects of exercise intervention on physical mobility in stroke patients: a scoping review and research progress.Frontiers in neurology · 2025Pooled it
- Proton-activated chloride channel 1 is essential for innate host defense against bacterial sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The perforant pathway and CA3-Schaffer collateral afferents coordinate to regulate spatial learning.Communications biology · 2026Article
- PAC regulates endo-, and exocytosis, and lysosomal-mitochondrial stress signaling in human mast cells.Cell communication and signaling : CCS · 2026Article
- Puromycin-sensitive aminopeptidase acts as an inhibitory auxiliary subunit of volume-regulated anion channels and regulates cGAMP transport.Molecular cell · 2025Article
- Puromycin-sensitive aminopeptidase acts as an inhibitory auxiliary subunit of volume-regulated anion channels.bioRxiv : the preprint server for biology · 2025Article
- Alternative splicing regulates PACC1 function and promotes acidosis-induced cytotoxicity.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Hippocampal long-term potentiation (LTP) and long-term depression (LTD) are forms of synaptic plasticity, thought to be the molecular basis of learning and memory, dependent on dynamic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) trafficking. Alteration of endosomal pH negatively affects synaptic transmission and neural development, but it is unclear how pH is involved in AMPAR trafficking. We show that the proton-activated chloride (PAC) channel localizes to early and recycling endosomes in neurons and prevents endosome hyper-acidification. Loss of PAC reduces AMPAR endocytosis during chemical LTD in primary neurons, while basal trafficking and LTP are unaffected. Pyramidal neuron-specific PAC knockout mice have impaired hippocampal LTD, but not LTP, and perform poorly in the Morris water maze reversal test, exhibiting impaired behavioral adaptation. We conclude that proper maintenance of endosomal pH by PAC in neurons is important during LTD to regulate AMPAR trafficking in a manner critical for animal physiology and behavior.
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