Study summary · research use only
Stimulus-specific enhancement in mouse visual cortex requires GABA but not VIP-peptide release from VIP interneurons
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This mouse study investigated stimulus-specific enhancement (SSE) in visual cortex (V1) following repeated exposure to a visual stimulus for as little as 1 h per day during locomotion-associated high-gain states. The researchers used genetic ablation to distinguish the roles of vasoactive intestinal peptide (VIP) and GABA, both released by VIP-positive interneurons. SSE was not impaired by VIP deletion but was prevented when GABA release from VIP cells was compromised. The authors suggest SSE may result from Hebbian mechanisms present in adult V1, and report that GABA release, rather than the VIP peptide, accounted for the neurons' action on this form of cortical plasticity.
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.NEW & NOTEWORTHY Many neurons package and release a peptide along with a conventional neurotransmitter. The conventional view is that such peptides exert late, slow effects on plasticity. We studied a form of cortical plasticity that depends on the activity of neurons that express both vasoactive intestinal peptide (VIP) and the inhibitory neurotransmitter GABA. GABA release accounted for their action on plasticity, with no effect of deleting the peptide on this phenomenon.
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