| Project/Area Number |
23790744
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General internal medicine (including Psychosomatic medicine)
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| Research Institution | Kochi University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 脳内大麻 / エンドカンナビノイド / 2-アラキドノイルグリセロール / カンナビノイドCB受容体 / 中枢性交感神経ー副腎髄質系 / グルタミン酸神経系 / 視床下部室傍核（PVN） / ストレス / 交感神経―副腎髄質系 / 中枢性交感神経―副腎髄質系 / 視床下部 / PVN / アラキドン酸 / モノアシルグリセロールリパーゼ / NMDA受容体 |
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| Research Abstract |
We examined central regulation mechanisms of sympatho-adrenomedullary (SA) outflow, which plays an important role in pathophysiological responses to stressors, regarding brain 2-arachidonoylglycerol (2-AG), an endogenous ligand for cannabinoid receptors (endocannabinoid, eCB), and the hypothalamic paraventricular nucleus (PVN), a regulatory center of the outflow. The results from the present studies suggest that (1) brain 2-AG can be metabolized to prostaglandin E2 (PGE2) glycerol ester, thereby activating the SA outflow as a precursor of PGE2, and that (2) brain eCB can be suppressively involved in the central SA outflow in the PVN by inhibiting glutamate release from the glutamatergic nerves innervating the PVN. These findings indicate a possibility that drugs activating brain eCB signals may be beneficial for clinical application to "stress-related disorders", such as hypertension, developed by high levels of stress-induced excess activation of the SA outflow.
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