Glutamatergic and dopaminergic contributions to rat bladder hyperactivity after cerebral artery occlusion

The contribution of glutamatergic and dopaminergic mechanisms to bladder hy peractivity after left middle cerebral artery occlusion was evaluated by de termining the effects of intravenous cumulative doses of an N-methyl-D-aspa rtate (NMDA) glutamatergic antagonist (MK-801) and D-1-selective (Sch-23390 ), Da-selective (sulpiride), or nonselective (haloperidol) dopaminergic ant agonists on bladder activity in sham-operated (SO) and cerebral-infarcted ( CI) rats. MK-801 (1 and 10 mg/kg) or sulpiride (3-30 mg/kg) significantly i ncreased bladder capacity (BC) in CI but decreased or had no effect, respec tively, on BC in SO. Sch-23390 (0.1-3 mg/kg) decreased BC in both SO and CI . In both CI and SO, low doses of haloperidol (0.1-1 mg/kg) increased BC, b ut a higher dose (3 mg/kg) reversed this effect. Administration of haloperi dol (0.3 mg/kg) or sulpiride (10 mg/kg) in combination with MK-801 (0.01-10 mg/kg) markedly increased BC in CI but produced small decreases or increas es in BC depending on the dose of MK-801 in SO. These results indicate that the bladder hyperactivity induced by cerebral infarction is mediated in pa rt by NMDA glutamatergic and D-2 dopaminergic excitatory mechanisms.