EEG-synchronizing effect of gamma-hydroxybutyrate and 1-hydroxy-3-amino-pyrrolidone-2 (HA-966) in relation to dopaminergic brain function.

The earlier finding that γ-hydroxybutyrate and HA-966-induced depression of the central nervous system was associated with the increase of dopamine concentration and block of its release, prompted this study of the influence which the monoaminergic system may have upon the electrocorticogram in rats.The synchronization induced by α-methyl-p-tyrosine began earlier than the decrease of the duration of arousal, indicating different sensitivities to the depressive drug action of structures responsible for synchronizing and for arousal.Five $\text{mg}\text{kg}$ HA-966 in diethyldithiocarbamate desynchronized animals increased the amplitude but the duration of arousal was unchanged. p-Chlorophenylalanine treatment of rats did not influence the synchronizing effect of HA-966 (10–20 $\text{mg}\text{kg}$) or the inhibitory effect upon the duration of arousal. Haloperidol (100 μg-4 $\text{mg}\text{kg}$) potentiated the synchronizing effect of y-hydroxybutyrate and HA-966. The number of phasic discharges in the electrocorticogram induced by treatment with anaesthetic doses of γ-hydroxybutyrate were increased by the low dose of haloperidol (100 $\text{μg}\text{kg}$), while the higher dose (4 $\text{mg}\text{kg}$) was ineffective.Animals with intact and lesioned substantia nigra compacta responded equally to the synchronizing activity of HA-966 and γ-hydroxybutyrate. Therefore, it is concluded that their effect is not due to the accumulation of dopamine in the nigrostriatal system.