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Mechanism of regulation of neuronal activity in the basolateral amygdala by medial prefrontal cortex

Research Project

Project/Area Number 14570952
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Psychiatric science
Research InstitutionTottori University (2003)
Okazaki National Research Institutes (2002)

Principal Investigator

KANEKO Koichi  Tottori University, Faculty of Medicine, Department of Neuropsychiatry, Assistant, 医学部, 助手 (50194907)

Project Period (FY) 2002 – 2003
Project Status Completed (Fiscal Year 2003)
Budget Amount *help
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
Keywordsamygdala / basolateral nucleus / GABA / regular-spiking / noradrenaline / nonselective cation channel / medial prefrontal cortex / α_1-adrenergic receptor / GABA作動性細胞 / Regular-spiling cell / フィードフォワード抑制 / 恐怖条件付け学習 / GABA作動性ニューロン / セロトニン
Research Abstract

To investigate the noradrenaline (NA) effects on medium-to large-sized GABAergic neurons, and also to identify the GABAergic cell types whose activity are regulated by projection from medial prefrontal cortex, we generated glutamate decarboxylase 67 (GAD67)-green fluorescent protein (GFP) knock-in mice, in which GFP was specifically expressed in GABAergic neurons. Using whole-cell patch-clamp recordings in vitro, three electrophysiologically distinct types of GABAergic neurons were identified in the BLA on the basis of the action potential firing pattern induced by depolarizing current injection : Type A-regular spiking (RS) cells, Type B-low threshold spiking (LTS), cells and Type C-fastspiking (FS) cells. Electrophysiological properties also showed difference among these three types of GABAergic neurons. We found that NA preferentially excited Type A-RS cells via α_1-adrenoceptors and augmented tonic inhibition while minimally affecting the other types of neurons. Averaged reversal potential of the net NA-induced, current was -31.3 ± 7.6 mV. Reducing the external Na^+ concentration to 27 mM shifted the reversal potential to more negative values and also revealed an additional reversal potential. These results indicate that the NA effect was, mediated by activation of nonselective cationic conductance and suppression of the resting K^+ conductance and that the NA effect on the neural activity of the BLA involves augmentation of GABAergic inhibition mediated by exciting a specific subpopulation of GABAergic interneurons. In addition, great majority of Type A cells receive monosynaptic input from medial prefrontal cortex (XX/YY), whereas Type B (XX/YY) and Type C (XX/YY) cells do it less frequently, suggesting a major role for Type A cells in feedforward inhibition of the activity in the BLA by medial prefrontal cortex

Report

(3 results)
  • 2003 Annual Research Report   Final Research Report Summary
  • 2002 Annual Research Report
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] Koichi Kaneko, kunihiko obata, Yuchio Yanagawa: "Ionic mechanism of noradrenergic excitation of regular-spiking GABAergic cells in basolateral amygdala"Neuroscience Research. Suppl.45. 49 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Koichi Kaneko, Kunihiko Obata, Yuchio Yanagawa: "Noradrenergic excitation of regular-spiking GABAergic cells in basolateral amygdala primarily via activation of Ca2+-dependent nonselective cation channels"Neuroscience Research. Suppl.46. 63 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] K.Kaneko, K.Obata, Y.Yanagawa: "Ionic mechanism of noradrenergic excitation of regular-spiking GABAergic cells in basolateral amygdala"Neuroscience Res.. 45. 49 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] K.Kaneko, K.Obata, Y.Yanagawa: "Noradrenergic excitation of regular-spiking GABAergic cells in basolateral amygdala primarily via activation of Ca2+-dependent nonselective cation channels"Neuroscience Res.. 46. 63 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2003 Final Research Report Summary
  • [Publications] Koichi Kaneko: "Noradrenergic excitation of regular-spiking GABAergic cells in basolateral amygdalavia an activation of Ca2+-dependent nonselective cation channels"Neuroscience Research. 46巻・S1. 63 (2003)

    • Related Report
      2003 Annual Research Report
  • [Publications] Koichi Kaneko: "Ionic mechanism of noradrenergic excitation of regular-spiking GABAergic cells in basolateral amygdala"Neuroscience Research. Supplement26(in press). (2002)

    • Related Report
      2002 Annual Research Report

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Published: 2002-04-01   Modified: 2016-04-21  

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