| Project/Area Number |
13671018
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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 | 宮崎医科大学 |
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Principal Investigator |
ISHIZUKA Yuta Miyazaki Medical College, Lecturer, 医学部, 講師 (20264377)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIDA Yasushi Miyazaki Medical College, Professor, 医学部, 教授 (20212897)
HASHIGUCHI Hiroyuki Miyazaki Medical College, Assistant, 医学部, 助手 (40305090)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2001: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | paraventricular nucleus / medial prefrontal cortex / interleukin-1β / nitric oxide / γ-aminobutyric acid(GABA) / 視床下部質傍核 / 内側前頭野 / 前頭前野 / マイクロダイアリシス |
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| Research Abstract |
We have suggested previously that intraperitoneal (I.p.) administration of interleukin-1β (IL-1β) increases nitric oxide (NO) levels in the hypothalamic paraventricular nucleus (PVN). Using an in vivo brain microdialysis technique, we measured extracellular levels of NO metabolites (Nox^-) in the hypothalamic PVN upon perfusion of selective γ-aminobutyric acid (GABA) receptor antagonist as well as agonist into the medial prefrontal cortex (mPFC) through a microdialysis probe. We examined the effects of selective GABAA receptor antagonist and agonist on IL-1β-induced NO releases in the PVN in conscious rats. Double immunostaining for Fos and neuronal nitric oxide synthase (nNOS) was also used to examine whether nNOS-immunoreactive neurons in the PVN are activated to express Fos immunoreactivity by I.p. injection of IL-Iβ in the rat. The elevated levels of Nox^- in the PVN after I.p. administration IL-1β (4μg/kg) were attenuated by perfusion of muscimol (50 μM), a GABAA receptor agonist, into the mPFC. We also examined the effect of GABAB receptor antagonist and agonist on IL-1β-induced NO releases in the PVN in conscious rats. Perfusion of baclofen (250 μM), a GABAB receptor agonist, into the mPFC had no effect on the elevated levels of Nox^- in the PVN after I.p administration IL-1β(4 μg/kg). Perfusion of saclofen (50 μM), a GABAB receptor antagonist, into the mPFC had no effect on the elevated levels of Nox^- in the PVN after I.p. administration IL-1β(4 μg/kg). Quantitative analysis revealed that some nNOS-positive PVN neurons are activated by IL-1β(4 μg/kg, I.p.) administration. These findings are likely to provide helpful clues to our understanding of the inhibitory modulation of IL-1β-induced NO metabolites releases in the PVN by GABAA and GABAB receptors in the mPFC.
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