| Co-Investigator(Kenkyū-buntansha) |
MAJIMA Takehiko Gunma University, Neuropsychiatry, Assistant, 医学部, 助手 (00312869)
IDA Itsuro Gunma University, Neuropsychiatry, Instructor, 医学部, 講師 (50251103)
FUKUDA Masato Gunma University, Neuropsychiatry, Associate Professor, 医学部, 助教授 (20221533)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Research Abstract |
To clarify a neuronal vulnerability in primary mood disorder, we have investigated if cytoarchitectural alterations would be observed in the left prefrontal cortex, BA 9 in postmortem brain tissue from subjects with primary mood disorder, who were under long-term treatment with antidepressant and mood stabilizers. The left prefrontal cortex, BA 9 is documented to be one of the pathophysiological brain regions, and we have clearly demonstrated that the lowered glucose uptake activity was estimated by FDG-PET, in the left prefrontal cortex, BA 9, in depressive state-depended manner. Reduction in the density of small cell neurons has been observed in layer II, but not in I, III, IV in the left BA 9. There are no changes in glial density and large neuronal cell density in the left BA 9, although the decrease was observed through the depth of cortex of BA 9, compared with normal controls. Interestingly, the number of serotonin (5-HT)-2A receptor immunorecative cells was significantly increased in layer II, but not in I, III, IV in the left BA 9 in postmortem brain from subjects with primary mood disorder. The density of 5-HT-2A receptor binding sites is well-known to be down-regulated after subchronic administration of antidepressant agents in rat cerebral cortex. Therefore, the layer II in the left prefrontal cortex, BA 9 is of special interest in the vulnerability in primary mood disorder and refractoriness to antidepressant treatment.
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