GABAergic contribution to rat bladder hyperactivity after middle cerebral artery occlusion

Citation
S. Kanie et al., GABAergic contribution to rat bladder hyperactivity after middle cerebral artery occlusion, AM J P-REG, 279(4), 2000, pp. R1230-R1238
Citations number
29
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
279
Issue
4
Year of publication
2000
Pages
R1230 - R1238
Database
ISI
SICI code
0363-6119(200010)279:4<R1230:GCTRBH>2.0.ZU;2-T
Abstract
To evaluate the influences of gamma-aminobutyric acid (GABA) mechanisms on bladder hyperactivity after left middle cerebral artery occlusion, cystomet ric recordings were obtained from unanesthetized female rats. Intracerebrov entricular administration of both muscimol (GABA(A) receptor agonist; 0.1-1 0 nmol) and baclofen (GABA(B) receptor agonist; 0.1-3 nmol) produced dose-d ependent 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 (GABA(A) receptor antagonist; 1 or 3 nmol) administration, BC in both SO an d CI rats first decreased and subsequently increased. An increase in urethr al pressure was observed after administration of bicuculline (3 nmol) but n ot with either muscimol or baclofen. Infarct volumes in muscimol-, bicucull ine-, or baclofen-treated rats were not significantly different from those of vehicle-treated rats. These results suggest that GABAergic mechanisms in hibit the micturition reflex at the supraspinal level but that this can cha nge as a result of CI.