This study presents the actions of risperidone (Risp) and haloperidol (Hal) on the behavioral effects elicited by ketamine (Ket) on open-field (OF), rota rod (RR) and tail suspension (TS) tests in mice. Male Swiss albino mice (25-30g) were used. Antipsychotics were administered alone (Risp: 0.1 or 0.2 mg/kg, ip; Hal: 0.1 and 0.2 mg/kg, ip) or thirty minutes before Ket (10 mg/Kg, ip). Ket increased (Ket: 63.3 ± 4.2) the locomotor activity compared to control, while neuroleptics decreased it (25.5 ± 4.2). Pretreatment with neuroleptics, in both doses, blocked hyperlocomotion caused by Ket. In RR, Ket decreased (Ket: 15 ± 4.1) the permanence time of the animals compared to control (Control: 59 ± 0.6), but this effect was not observed when neuroleptics were administered alone. Pretreatment with neuroleptics reverted the effect of Ket only in the RR. While Ket (17.3 ± 5.6) decreased the time of immobility in the tail suspension test compared to the control (80.2 ± 10.2), the pretreatment with neuroleptics reverted this mobility. The action of neuroleptics in this model made possible the blockade of the effects caused by acute administration of Ket. Thus, the mechanism of action of ketamine may involve the dopaminergic system.

Aminophylline is a complex of theophylline-ethylenediamine, where theophylline is the main component. Theophylline is a methyxanthine and besides inhibiting phosphodiesterase enzymes, it is also a nonselective adenosine antagonist. Several reports suggested the involvement of the brain adenosinergic system in the ethanol-induced motor incoordination. Thus, the objective of this work was to study the effects of the interaction of ethanol with aminophylline as assessed by behavioral tests in mice. Eight groups of male Swiss mice were used. The animals were treated with either distilled water (control) or ethanol (E; 2, 4, and 6 g/kg, orally) for 5 days, or with distilled water for 4 days, and on the fifth day with aminophylline (A; 5 and 10 mg/kg, intraperitoneally). In the association groups (association protocols), the animals were treated with ethanol (E; 6 g/kg, orally) for 4 days, and on the fifth day received aminophylline (A; 10 mg/kg, intraperitoneally), 30 min after the last ethanol administration (first protocol, E/A). In the second association protocol (A/E), ethanol was administered for 4 days, and on the fifth day the animals received aminophylline (A; 10 mg/kg, intraperitoneally), followed again by ethanol (E; 6 g/kg, orally) administration, 30 min later. E (6 g/kg) evoked a central nervous system depressor effect, by decreasing both the locomotor activity and rearing in the open field test, and A (5 and 10 mg/kg) showed opposite effects. However, the E/A or A/E associations blocked the ethanol effect. In the rota rod test, ethanol presented a muscular relaxant effect, which was decreased in both association protocols. In the tail suspension test, while the E/A association decreased immobility, A/E association increased it, as compared with controls. In conclusion, the effects of ethanol were inhibited by its association with aminophylline, suggesting that ethanol acts on the adenosine neurotransmission.