| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Research Abstract |
Peripheral inflammation induced by bacterial endotoxin induces cytokine expression in the brain, anorexial and fever responses. Direct electrical stimulation of the afferent vagus nerves itself can induce production of IL-1β in brain and activate the HPA axis. Therefore, the afferent vagus nerve may play an important role in transmitting peripheral signals to the brain in the acute phase of infection and inflammation. Increasing evidence has suggested that leptin, the product of the ob gene may interact with cytokines in immune system. Peripherally applied leptin increased IL-1β transcripts in the hypothalamus, the hippocampus, the cortex, the cerebellum and the brainstem. Leptin increased the expression of IL-1β mRNA in mouse primary cultured glial cells, indicating that tone of the target cells of the leptin-induced IL-1β transcript may be a gial cells. Leptin applied to the db/db mice, which lack functional Ob-Rb receptor, increased IL-1β mRNA levels in the hypothalamus to similar e
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xtents as normal mice. These results indicate that the leptin-induced cytokine expression in the brain probably be mediated through short isoform of leptin receptor. We examined whether leptin -induced IL-1β induction is mediating through activating vagal afferent nerve activity. Since vagotomy did not modulate leptin-inducede IL-1β expression in the brain, it is suggested that circulating leptin directly acts in the brain and induces IL-1β transcript via short isoform of leptin receptor.
The senescence-accelerated mouse (SAM) is known to be a marine mode, for accelerated aging. The SAMP8 strain shows age-related deterioration of learning and memory. In the brain of 10 months old SAMP8, the expression of IL-1β in the hippocampus and hypothalamus, and in TNF-α and IL-6 in the cerebral cortex and the hippocampus were significantly elevated. Increases in expression of proinflammatory cytokines in the brain may be involved in the age-related neurl dysfunction and/or learning deficiency in SAMPS. Less
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