A cortical disinhibitory circuit for enhancing adult plasticity

eLife - Tập 4
Yu Fu1, Megumi Kaneko1, Yunshuo Tang2,3,4, Arturo Alvarez‐Buylla2,4, Michael P. Stryker1
1Center for Integrative Neuroscience, Department of Physiology, University of California, San Francisco, San Francisco, United States
2Department of Neurological Surgery, University of California, San Francisco, San Francisco, United States
3Medical Scientist Training Program, Biomedical Science Program, University of California, San Francisco, San Francisco, United States
4The Eli and Edythe Broad Center of Regeneration Medicine, University of California, San Francisco, San Francisco, United States

Tóm tắt

The adult brain continues to learn and can recover from injury, but the elements and operation of the neural circuits responsible for this plasticity are not known. In previous work, we have shown that locomotion dramatically enhances neural activity in the visual cortex (V1) of the mouse (<xref ref-type="bibr" rid="bib27">Niell and Stryker, 2010</xref>), identified the cortical circuit responsible for this enhancement (<xref ref-type="bibr" rid="bib5">Fu et al., 2014</xref>), and shown that locomotion also dramatically enhances adult plasticity (<xref ref-type="bibr" rid="bib19">Kaneko and Stryker, 2014</xref>). The circuit that is responsible for enhancing neural activity in the visual cortex contains both vasoactive intestinal peptide (VIP) and somatostatin (SST) neurons (<xref ref-type="bibr" rid="bib5">Fu et al., 2014</xref>). Here, we ask whether this VIP-SST circuit enhances plasticity directly, independent of locomotion and aerobic activity. Optogenetic activation or genetic blockade of this circuit reveals that it is both necessary and sufficient for rapidly increasing V1 cortical responses following manipulation of visual experience in adult mice. These findings reveal a disinhibitory circuit that regulates adult cortical plasticity.

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