Table 6

Effects of amisulpride on dopamine synthesis in the rat brain after blockade of impulse flow

DrugDose (mg/kg i.p.)Dopa Level (% control)
StriatumLimbic System
Control100  ± 2100  ± 4
+ γ-Hydroxy-butyrate750225  ± 6115  ± 5
  + Amisulpride0.5209  ± 20101  ± 5
1224  ± 22123  ± 4
2193  ± 11114  ± 6
5184  ± 27114  ± 6
20198  ± 17127  ± 5
75208  ± 26139  ± 13*
Control100  ± 8100  ± 5
+ γ-Hydroxy-butyrate750199  ± 24110  ± 6
  + Haloperidol0.03225  ± 16118  ± 7
0.1288  ± 25* 137  ± 8
0.3281  ± 28* 143  ± 8*

Rats received NSD-1015 (100 mg/kg) 90 min after the administration of amisulpride or its vehicle control and were sacrificed 30 min thereafter. γ-Hydroxy-butyric acid was administered 45 min before sacrifice. Because the data for amisulpride derive from multiple experiments, they are expressed as a percentage of the control value for each experiment. Mean control dopa levels varied from 1038 ± 80 to 1451 ± 86 and from 592 ± 19 to 710 ± 33 ng/g wet tissue weight for the striatum and limbic system, respectively, in the case of amisulpride. In the case of haloperidol, control dopa levels were 1038 ± 80 and 619 ± 30 ng/g wet tissue weight for the striatum and limbic system, respectively. Shown are the mean and S.E.M. (n = 3–7/group).

  • * P < .05 vs. the γ-hydroxy-butyrate group.