Adenosine suppresses neuronal death induced by experimental ischemia in lumbar motoneurones
| Project/Area Number |
18591641
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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 |
Orthopaedic surgery
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| Research Institution | Wakayama Medical University |
|---|
Principal Investigator |
YOSHIDA Munehito Wakayama Medical University, Medical, professor (60201018)
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|---|
| Co-Investigator(Kenkyū-buntansha) |
NAKATSUKA Terumasa Saga University, Medical, associate professor (30380752)
MIYAZAKI Nobuyuki Wakayama Medical University, 医学部, instructor (90438276)
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|---|
| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥3,810,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥210,000)
Fiscal Year 2007: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2006: ¥2,900,000 (Direct Cost: ¥2,900,000)
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|---|
| Keywords | spinal cord injury / neuroscience / neurophysiology / signal / cell・tissue / 細胞・組織 / シグナル伝達 |
|---|
| Research Abstract |
Although adenosine is an important neuromodulator, its role in modulating motor functions at the level of the spinal cord has been poorly understood. In the present study, we investigated the effects of adenosine on excitatory synaptic transmission and neuronal death induced by experimental ischaemia by using whole-cell patch-clamp recordings from lamina IX neurones in spinal cord slices. Adenosine significantly decreased the frequency of miniature excitatory postsynaptic currents (mEPSCs) in almost all neurones examined that could be mimicked by an A_1 receptor agonist, CPA, and inhibited by an A_1 receptor antagonist, DPCPX. Interestingly, adenosine increased mEPSC frequency in the presence of DPCPX in a subpopulation of neurones recorded. In those neurones, an A_2A receptor agonist, CGS21680, also increased mEPSC frequency. Moreover, adenosine induced an outward current at a holding potential of -50 mV in the majority of neurones recorded. The adenosine-induced outward current is mimicked by CPA, but not CGS21680 and inhibited by DPCPX. Surperfusing ischaemia simulating medium (ISM) generated an agonal inward current in all of the neurones tested. The latencies of the inward currents induced by ISM were significantly prolonged by adenosine or CPA, but not CGS21680. These results suggest that adenosine receptors are functionally expressed in both the pre- and postsynaptic sites of lamina IX neurones and that their activation may exert multiple effects on motor functions. Moreover, this study has provided a cellular basis for an involvement of A_1 receptors in the neuroprotective actions of adenosine.
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Report
(3 results)
Research Products
(87 results)
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[Book] 大脳皮質の機能局在2007
Author(s)
中塚 映政
Total Pages
4
Publisher
日本医事新報
Description
「研究成果報告書概要(和文)」より
Related Report
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