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Am J Physiol Regul Integr Comp Physiol 279: R1230-R1238, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 4, R1230-R1238, October 2000

GABAergic contribution to rat bladder hyperactivity after middle cerebral artery occlusion

Sayoko Kanie1,2, Osamu Yokoyama1, Kazuto Komatsu1, Koichi Kodama1, Satoshi Yotsuyanagi1, Susumu Niikura1, Yasuhiro Nagasaka1, Ken-Ichi Miyamoto2, and Mikio Namiki1

1 Department of Urology, Kanazawa University School of Medicine, and 2 Department of Pharmacology and Pharmaceutics, Graduate School of Natural Science and Technology, Kanazawa University, Ishikawa 920-8641, Japan

To evaluate the influences of gamma -aminobutyric acid (GABA) mechanisms on bladder hyperactivity after left middle cerebral artery occlusion, cystometric recordings were obtained from unanesthetized female rats. Intracerebroventricular administration of both muscimol (GABAA receptor agonist; 0.1-10 nmol) and baclofen (GABAB receptor agonist; 0.1-3 nmol) produced dose-dependent inhibitions of micturition with increases in bladder capacity (BC). The effects of high doses (1-10 nmol) were similar in sham-operated (SO) and cerebral-infarcted (CI) rats. However, lower doses of muscimol (0.1 or 0.3 nmol) and baclofen (0.1 nmol) reduced BC in CI rats. After bicuculline (GABAA receptor antagonist; 1 or 3 nmol) administration, BC in both SO and CI rats first decreased and subsequently increased. An increase in urethral pressure was observed after administration of bicuculline (3 nmol) but not with either muscimol or baclofen. Infarct volumes in muscimol-, bicuculline-, or baclofen-treated rats were not significantly different from those of vehicle-treated rats. These results suggest that GABAergic mechanisms inhibit the micturition reflex at the supraspinal level but that this can change as a result of CI.

GABA or gamma -aminobutyric acid; micturition reflex; cerebral infarction


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