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Developmental profile of GABAA-mediated synaptic transmission in pyramidal cells of the somatosensory cortex

Authors

  • Masayuki Kobayashi,

    1. Department of Pharmacology, Nihon University School of Dentistry, Kanda-Surugadai 1-8-13, Chiyoda-ku, Tokyo 101-8310, Japan
    2. Department of System Neuroscience, Osaka City University Graduate School of Medicine, Abeno-ku, Osaka 545-8585, Japan
    3. Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Yamadaoka 1-8, Suita, Osaka 565-0871, Japan
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  • Tomohiro Hamada,

    1. Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Yamadaoka 1-8, Suita, Osaka 565-0871, Japan
    2. Department of Maxilofacial Surgery, Osaka University Graduate School of Dentistry, Yamadaoka, Suita, Osaka, Japan
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  • Mikihiko Kogo,

    1. Department of Maxilofacial Surgery, Osaka University Graduate School of Dentistry, Yamadaoka, Suita, Osaka, Japan
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  • Yuchio Yanagawa,

    1. Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan
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  • Kunihiko Obata,

    1. Neuronal Circuit Mechanisms Research Group, RIKEN Brain Science Institute, Hirosawa, Wako, Japan
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  • Youngnam Kang

    1. Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Yamadaoka 1-8, Suita, Osaka 565-0871, Japan
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Dr M. Kobayashi, 1Department of Pharmacology, as above.
E-mail: kobayashi-ms@dent.nihon-u.ac.jp

Abstract

Inhibitory synaptic transmission mediated by γ-aminobutyric acid (GABA)A receptors is involved in regulation of experience-dependent cortical plasticity. However, little information is available on their presynaptic and postsynaptic developmental profiles. The present study aims to investigate the developmental changes of miniature and unitary inhibitory postsynaptic currents (mIPSCs and uIPSCs) in mouse barrel cortex. mIPSCs recorded from supragranular pyramidal neurons showed a gradual increase in frequency during postnatal days 6–15 (PD6–15) followed by a marked increase at PD16–20, and mIPSCs frequency reached a plateau at about PD21–30. The amplitude of mIPSCs showed a transient decrease at PD10–12 followed by an increase during PD13–30, and reached a plateau at about PD30. Their decay time constant progressively decreased during the first 30 days postnatally, and reached a steady level at about PD30. Paired recordings from interneurons and synaptically coupled target pyramidal cells revealed that uIPSC amplitude increased with age up to PD30. In contrast, failure rate and coefficient of variation decreased during PD7–15 and showed little change at a later stage. Short-term depression induced by presynaptic stimulation at 33 Hz progressively decreased during PD6–20, and was stabilized at about PD21–30. Quantal analysis revealed that the number of release sites increased with age up to PD30, while the release probability increased during PD6–12 and then reached a plateau level. These results suggest that the number of release sites and release probability of GABA and GABAA-mediated IPSC kinetics show distinct developmental profiles, which could play roles in regulating the onset and offset of critical periods for experience-dependent cortical plasticity.

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