Attentional effects on local V1 microcircuits explain selective V1-V4 communication
preprint
OA: gold
publisher-OA-unknown
Abstract
ABSTRACT Selective attention implements preferential routing of attended stimuli, likely through increasing the influence of the respective synaptic inputs on higher-area neurons. As the inputs of competing stimuli converge onto postsynaptic neurons, presynaptic circuits might offer the best target for attentional top-down influences. If those influences enabled presynaptic circuits to selectively entrain postsynaptic neurons, this might explain selective routing. Indeed, when two visual stimuli induce two gamma rhythms in V1, only the gamma induced by the attended stimulus entrains gamma in V4. Here, we modeled induced responses with a Dynamic Causal Model for Cross-Spectral Densities and found that selective entrainment can be explained by attentional modulation of intrinsic V1 connections. Specifically, local inhibition was decreased in the granular input layer and increased in the supragranular output layer of the V1 circuit that processed the attended stimulus. Thus, presynaptic attentional influences and ensuing entrainment were sufficient to mediate selective routing. HIGHLIGHTS We model selective visual attention in macaques using Dynamic Causal Modeling. Intrinsic V1 modulation can explain attention effects in V1-V4 communication. Modulation of superficial and granular inhibition is key to induce the effects. Those modulations increase V1-V4 communication in a feedforward manner. GRAPHICAL ABSTRACT
My notes (saved in your browser only)
Citation neighborhood (no data yet)
We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.
Source provenance
- europepmc
- last seen: 2026-05-19T01:45:01.086888+00:00
- unpaywall
- last seen: 2026-05-21T05:10:58.409756+00:00
License: publisher-OA-unknown
· commercial use NOT OK
· attribution required