ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Vision loss shifts the balance of feedforward and intracortical circuits in opposite directions in mouse primary auditory and visual cortices.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed.
- Article
- Excitatory and inhibitory networks diverge following early blindness.Cerebral cortex (New York, N.Y. : 1991) · 2026Article
- Cortical functional connectivity in mouse models of early blindness: enucleation vs. anophthalmia.Cerebral cortex (New York, N.Y. : 1991) · 2026Article
- Post-Critical Period Transcriptional and Physiological Adaptations of Primary Sensory Cortex after Sensory Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Rapid plasticity of default-mode local network architectures following adult-onset blindness.Cell reports · 2026Article
- Functional reorganization of the visual cortex in blindness: a connectivity perspective.Frontiers in human neuroscience · 2026Review
- Reactivated thalamocortical plasticity alters neural activity in sensory-motor cortex during post-critical period.Progress in neurobiology · 2025Article
- Excitatory/Inhibitory imbalance as a mechanism linking autism and sleep problems.Current opinion in neurobiology · 2025Review
- Spatial Mapping of Activity Changes across Sensory Areas Following Visual Deprivation in Adults.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Brief periods of visual deprivation in adults increase performance on auditory tasks.iScience · 2024Article
- Dark exposure reduces high-frequency hearing loss in C57BL/6J mice.bioRxiv : the preprint server for biology · 2024Article
- Transcranial Low-Intensity Focused Ultrasound Stimulation of the Visual Thalamus Produces Long-Term Depression of Thalamocortical Synapses in the Adult Visual Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Selective plasticity of fast and slow excitatory synapses on somatostatin interneurons in adult visual cortex.Nature communications · 2023Article
- An Animal Model of Neonatal Intensive Care Unit Exposure to Light and Sound in the Preterm Infant.Integrative and comparative biology · 2023Article
- Crossmodal plasticity in hearing loss.Trends in neurosciences · 2023Review
- Visual Cortical Plasticity: Molecular Mechanisms as Revealed by Induction Paradigms in Rodents.International journal of molecular sciences · 2023Review
- Homeostatic regulation through strengthening of neuronal network-correlated synaptic inputs.eLife · 2022Article
- Synaptic Remodeling of the Auditory Cortex Following Bilateral Blindness: Evidence of Cross-modal Plasticity.Experimental neurobiology · 2022Article
- Visual Deprivation Selectively Reduces Thalamic Reticular Nucleus-Mediated Inhibition of the Auditory Thalamus in Adults.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Homeostatic plasticity and excitation-inhibition balance: The good, the bad, and the ugly.Current opinion in neurobiology · 2022Review
4 more citing papers are in PubMed but not listed here.
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6 authors.
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Abstract
Loss of a sensory modality leads to widespread changes in synaptic function across sensory cortices, which are thought to be the basis for cross-modal adaptation. Previous studies suggest that experience-dependent cross-modal regulation of the spared sensory cortices may be mediated by changes in cortical circuits. Here, we report that loss of vision, in the form of dark exposure (DE) for 1 week, produces laminar-specific changes in excitatory and inhibitory circuits in the primary auditory cortex (A1) of adult mice to promote feedforward (FF) processing and also strengthens intracortical inputs to primary visual cortex (V1). Specifically, DE potentiated FF excitatory synapses from layer 4 (L4) to L2/3 in A1 and recurrent excitatory inputs in A1-L4 in parallel with a reduction in the strength of lateral intracortical excitatory inputs to A1-L2/3. This suggests a shift in processing in favor of FF information at the expense of intracortical processing. Vision loss also strengthened inhibitory synaptic function in L4 and L2/3 of A1, but via laminar specific mechanisms. In A1-L4, DE specifically potentiated the evoked synaptic transmission from parvalbumin-positive inhibitory interneurons to principal neurons without changes in spontaneous miniature IPSCs (mIPSCs). In contrast, DE specifically increased the frequency of mIPSCs in A1-L2/3. In V1, FF excitatory inputs were unaltered by DE, whereas lateral intracortical connections in L2/3 were strengthened, suggesting a shift toward intracortical processing. Our results suggest that loss of vision produces distinct circuit changes in the spared and deprived sensory cortices to shift between FF and intracortical processing to allow adaptation.
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