2015 Fiscal Year Final Research Report
Plastic changes in transmission of neuropeptide and metabotropic glutamate related to voiding dysfunction after chronic spinal cord injury
Project/Area Number |
25462507
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Urology
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Research Institution | University of Yamanashi |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
KIRA Satoru 山梨大学, 総合研究部, 助教 (10530115)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | 下部尿路機能 / 膀胱 / 外尿道括約筋 / マウス / 排尿障害 / 脊髄損傷 / 興奮性グルタミン酸受容体 / 神経ペプチド |
Outline of Final Research Achievements |
We compared the lower-urinary-tract function of the wild type (WT) spinal cord injured mouse and the metabotropic glutamate receptor subtype 1a (mGluR1a-KO) gene deficit spinal cord injured mouse, using a cystometrogram and external urethral sphincter (EUS) electromyogram (EMG). The mGluR1a-KO presented more marked detrusor-sphincter dyssynergia (DSD) compared with WT. The mGluR5 antagonist increased the occurrence rate of DSD in the WT spinal cord injured mouse. The above results suggest that the neural transmission via mGluR1a and mGluR5 is involved in anti-DSD in urinary voiding dysfunction after spinal cord injury.
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Free Research Field |
排尿機能学
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