2003 Fiscal Year Final Research Report Summary
Mechanism of regulation of neuronal activity in the basolateral amygdala by medial prefrontal cortex
| Project/Area Number |
14570952
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Tottori University (2003)
Okazaki National Research Institutes (2002) |
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Principal Investigator |
KANEKO Koichi Tottori University, Faculty of Medicine, Department of Neuropsychiatry, Assistant, 医学部, 助手 (50194907)
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| Project Period (FY) |
2002 – 2003
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| Keywords | amygdala / basolateral nucleus / GABA / regular-spiking / noradrenaline / nonselective cation channel / medial prefrontal cortex / α_1-adrenergic receptor |
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| 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
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