title: Brief Dark Exposure Reduces Tonic Inhibition in Visual Cortex.
abstract: Tonic inhibition mediated by extrasynaptic GABA(A) receptors (GABARs) sensing ambient levels of GABA can profoundly alter the membrane input resistance to affect cellular excitability. Therefore, regulation of tonic inhibition is an attractive mechanism to control the levels of cortical firing. In cortical pyramidal cells, tonic inhibition is regulated by age and several neurotransmitters and is affected by stroke and epilepsy. However, the possible role of sensory experience has not been examined. Here, we report that a brief 2-day exposure to dark reduces by 1/3 the inhibitory tonic conductance recorded in layer II/III pyramidal cells of the mouse juvenile (postnatal day 12-27) visual cortex. In these cells, tonic inhibition is carried primarily by GABARs containing the δ subunit. Consistently, the dark exposure reduction in conductance was associated with a reduction in δ subunit levels, which were not affected in control frontal cortex. We propose that a deprivation-induced reduction in tonic inhibition might serve a homeostatic function by increasing the firing levels of cells in deprived cortical circuits.
authors.affiliation: The Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218, Program in Neuroscience, Hussman Institute for Autism, Baltimore, Maryland 21201.
authors.forename: Shiyong
authors.identifier: http://orcid.org/0000-0003-2976-5798
authors.initials: S
authors.lastname: Huang
authors.affiliation: Department of Pharmacology and Experimental Therapeutics, Laboratory of Translational Epilepsy, and Program in Biomolecular Pharmacology and Biomedical Neuroscience, Boston University School of Medicine, Boston, Massachusetts 02118, and.
authors.forename: Kristen
authors.identifier: http://orcid.org/0000-0001-6347-3719
authors.initials: K
authors.lastname: Hokenson
authors.affiliation: Department of Pharmacology and Experimental Therapeutics, Laboratory of Translational Epilepsy, and.
authors.forename: Sabita
authors.initials: S
authors.lastname: Bandyopadhyay
authors.affiliation: Department of Pharmacology and Experimental Therapeutics, Laboratory of Translational Epilepsy, and.
authors.forename: Shelley J
authors.initials: SJ
authors.lastname: Russek
authors.affiliation: The Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218, Department of Neuroscience, Johns Hopkins University, Baltimore, Maryland 21205 kirkwood@jhu.edu.
authors.forename: Alfredo
authors.identifier: http://orcid.org/0000-0001-9148-9742
authors.initials: A
authors.lastname: Kirkwood
mesh_terms: D000818:Animals; D003624:Darkness; D004558:Electric Stimulation; D005260:Female; D018682:GABA Agents / Q000494:pharmacology; D066298:In Vitro Techniques; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology*; D011963:Receptors, GABA-A / Q000378:metabolism; D014793:Visual Cortex / Q000166:cytology* / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
chemical_list: D018682:GABA Agents; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid
keywords: extrasynaptic receptors; layer 2/3; pyramidal cells; δ-GABAA receptor