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A modified water-lick conflict paradigm is described, using trained rats for up to 35 weekly test sessions under 48 h of water deprivation. The rats rapidly became maximally suppressed by the punishment. This suppression was attenuated by the anxiolytics lorazepam, diazepam, phenobarbital, and meprobamate. The potentially anxiolytic drug CL 218872 and the anticonvulsant drug valproate sodium were also active. The antiserotonin drugs methysergide, cyproheptadine, cinanserin and parachlorophenylalanine were all inactive, as were several several other distinct classes of psychotropic drugs including propranolol, clonidine, THIP, theophylline, chlorpromazine, paroxetine and ethanol. The paradigm proved reliable, reproducible and useful for large scale investigations. Furthermore, it may provide means for detailed neuropharmacological and anatomical studies.

A new phenylpiperidine derivative, FG4963, and several tricyclic antidepressants were compared in various in vitro and in vivo tests for central 5HT- and NA-uptake inhibition. FG4963 was found to be a 5HT-pump blocker with activity similar to that of chlorimipramine. FG4963 inhibited NA-uptake less than the most potent tricyclic thymoleptics. In contrast to imipramine derivatives FG4963 was a weak inhibitor of peripheral NA-uptake. FG4963 seems to produce central 5HT-potentiation without affecting organ functions regulated by the autonomic nervous system as much as tricyclic antidepressants.

1-Tryptophan was administered to rats pretreated with selective inhibitors of the A and B forms of MAO deprenyl, a selective inhibitor of MAO-B, produced minor changes in behaviour and in the concentrations of apparent 5-HT and 5-HAA in brain. High doses of clorgyline, a selective inhibitor MAO-A, produced a characteristic stereotyped syndrome of hypermotility and tremor as well as an increase in apparent 5-HT and a decrease in apparent 5-HIAA in brain. Small doses of deprenyl and clorgyline in combination, but not singly, produced maximal effects on behaviour as well as on the concentrations of apparent 5-HT and 5-HIAA in brain. Maximum behavioural and biors before the other. It is concluded that the syndrome may be dependent on the formation of an N-substituted derivative of 5-HT which is at least partly deaminated by MAO-B. Alternatively, the syndrome may be dependent on a sufficiently high concentration of 5-HT in a special compartment where it is partly deaminated by MAO-B.