ArticleJournal of neurophysiology2024
Stimulus-specific enhancement in mouse visual cortex requires GABA but not VIP-peptide release from VIP interneurons.
Article in Journal of neurophysiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Visual experience drives functional reorganization of cortical GABAergic circuits.bioRxiv : the preprint server for biology · 2026Article
- GABAergic signaling by VIP interneurons gates running-dependent visual recovery in the adult brain.bioRxiv : the preprint server for biology · 2025Article
- Understanding amblyopia from the perspective of neurovascular units: changes in the retina and brain.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
When adult mice are repeatedly exposed to a particular visual stimulus for as little as 1 h per day for several days while their visual cortex (V1) is in the high-gain state produced by locomotion, that specific stimulus elicits much stronger responses in V1 neurons for the following several weeks, even when measured in anesthetized animals. Such stimulus-specific enhancement (SSE) is not seen if locomotion is prevented. The effect of locomotion on cortical responses is mediated by vasoactive intestinal peptide (VIP) positive interneurons, which can release both the peptide and the inhibitory neurotransmitter GABA. Previous studies have examined the role of VIP-ergic interneurons, but none have distinguished the individual roles of peptide from GABA release. Here, we used genetic ablation to determine which of those molecules secreted by VIP-ergic neurons is responsible for SSE. SSE was not impaired by VIP deletion but was prevented by compromising release of GABA from VIP cells. This finding suggests that SSE may result from Hebbian mechanisms that remain present in adult V1.
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Registered trials
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