PMID- 25100608 OWN - NLM STAT- MEDLINE DCOM- 20141003 LR - 20211021 IS - 1529-2401 (Electronic) IS - 0270-6474 (Print) IS - 0270-6474 (Linking) VI - 34 IP - 32 DP - 2014 Aug 6 TI - Rebound potentiation of inhibition in juvenile visual cortex requires vision-induced BDNF expression. PG - 10770-9 LID - 10.1523/JNEUROSCI.5454-13.2014 [doi] AB - The developmental increase in the strength of inhibitory synaptic circuits defines the time window of the critical period for plasticity in sensory cortices. Conceptually, plasticity of inhibitory synapses is an attractive mechanism to allow for homeostatic adaptation to the sensory environment. However, a brief duration of visual deprivation that causes maximal change in excitatory synapses produces minimal change in inhibitory synaptic transmission. Here we examined developmental and experience-dependent changes in inhibition by measuring miniature IPSCs (mIPSCs) in layer 2/3 pyramidal neurons of mouse visual cortex. During development from postnatal day 21 (P21) to P35, GABAA receptor function changed from fewer higher-conductance channels to more numerous lower-conductance channels without altering the average mIPSC amplitude. Although a week of visual deprivation did not alter the average mIPSC amplitude, a subsequent 2 h exposure to light produced a rapid rebound potentiation. This form of plasticity is restricted to a critical period before the developmental change in GABAergic synaptic properties is completed, and hence is absent by P35. Visual experience-dependent rebound potentiation of mIPSCs is accompanied by an increase in the open channel number and requires activity-dependent transcription of brain-derived neurotrophic factor (BDNF). Mice lacking BDNF transcription through promoter IV did not show developmental changes in inhibition and lacked rebound potentiation. Our results suggest that sensory experience may have distinct functional consequences in normal versus deprived sensory cortices, and that experience-dependent BDNF expression controls the plasticity of inhibitory synaptic transmission particularly when recovering vision during the critical period. CI - Copyright (c) 2014 the authors 0270-6474/14/3410770-10$15.00/0. FAU - Gao, Ming AU - Gao M AD - The Solomon H. Snyder Department of Neuroscience, The Zanvyl-Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218, Department of Biology, University of Maryland, College Park, Maryland 20742. FAU - Maynard, Kristen R AU - Maynard KR AD - Lieber Institute for Brain Development, Baltimore, Maryland 21205, and. FAU - Chokshi, Varun AU - Chokshi V AD - The Solomon H. Snyder Department of Neuroscience, The Zanvyl-Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218. FAU - Song, Lihua AU - Song L AD - The Solomon H. Snyder Department of Neuroscience, The Zanvyl-Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218, Department of Biology, University of Maryland, College Park, Maryland 20742. FAU - Jacobs, Cara AU - Jacobs C AD - Department of Biology, University of Maryland, College Park, Maryland 20742. FAU - Wang, Hui AU - Wang H AD - The Solomon H. Snyder Department of Neuroscience, The Zanvyl-Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218. FAU - Tran, Trinh AU - Tran T AD - The Solomon H. Snyder Department of Neuroscience, The Zanvyl-Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218. FAU - Martinowich, Keri AU - Martinowich K AUID- ORCID: 0000-0002-5237-0789 AD - Lieber Institute for Brain Development, Baltimore, Maryland 21205, and Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205. FAU - Lee, Hey-Kyoung AU - Lee HK AD - The Solomon H. Snyder Department of Neuroscience, The Zanvyl-Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218, Department of Biology, University of Maryland, College Park, Maryland 20742, heykyounglee@jhu.edu. LA - eng GR - R01 EY014882/EY/NEI NIH HHS/United States GR - R01-EY14882/EY/NEI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural PT - Research Support, Non-U.S. Gov't PL - United States TA - J Neurosci JT - The Journal of neuroscience : the official journal of the Society for Neuroscience JID - 8102140 RN - 0 (Brain-Derived Neurotrophic Factor) RN - EC 4.1.1.15 (Glutamate Decarboxylase) RN - EC 4.1.1.15 (glutamate decarboxylase 2) SB - IM MH - Age Factors MH - Animals MH - Animals, Newborn MH - Biophysics MH - Brain-Derived Neurotrophic Factor/genetics/*metabolism MH - Electric Stimulation MH - Gene Expression Regulation, Developmental/genetics MH - Glutamate Decarboxylase/metabolism MH - In Vitro Techniques MH - Inhibitory Postsynaptic Potentials/drug effects/genetics MH - Mice MH - Mice, Inbred C57BL MH - Mice, Transgenic MH - Microscopy, Confocal MH - Neural Inhibition/drug effects/genetics/*physiology MH - Neurons/drug effects/*physiology MH - Patch-Clamp Techniques MH - Sensory Deprivation/physiology MH - Vision, Ocular/*physiology MH - Visual Cortex/*cytology PMC - PMC4200113 OTO - NOTNLM OT - BDNF OT - activity-dependent OT - critical period OT - mIPSC OT - potentiation OT - visual cortex EDAT- 2014/08/08 06:00 MHDA- 2014/10/04 06:00 PMCR- 2015/02/06 CRDT- 2014/08/08 06:00 PHST- 2014/08/08 06:00 [entrez] PHST- 2014/08/08 06:00 [pubmed] PHST- 2014/10/04 06:00 [medline] PHST- 2015/02/06 00:00 [pmc-release] AID - 34/32/10770 [pii] AID - 5454-13 [pii] AID - 10.1523/JNEUROSCI.5454-13.2014 [doi] PST - ppublish SO - J Neurosci. 2014 Aug 6;34(32):10770-9. doi: 10.1523/JNEUROSCI.5454-13.2014.