Rebound Potentiation of Inhibition in Juvenile Visual Cortex Requires Vision-Induced BDNF Expression
| Autor: | Lihua Song, Trinh T. Tran, Varun Chokshi, Kristen R. Maynard, Hui Wang, Keri Martinowich, Hey Kyoung Lee, Ming Gao, Cara Jacobs |
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| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
Patch-Clamp Techniques
Biophysics Mice Transgenic Neurotransmission In Vitro Techniques Inhibitory postsynaptic potential Mice Metaplasticity Animals Sensory deprivation Vision Ocular Visual Cortex Brain-derived neurotrophic factor Neurons Microscopy Confocal Glutamate Decarboxylase General Neuroscience Brain-Derived Neurotrophic Factor Age Factors Gene Expression Regulation Developmental Long-term potentiation Neural Inhibition Articles Electric Stimulation Mice Inbred C57BL Animals Newborn Inhibitory Postsynaptic Potentials Synaptic plasticity Excitatory postsynaptic potential Sensory Deprivation Psychology Neuroscience |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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