Central N omega-nitro-L-arginine Methyl Ester Does not Influence Lithium-induced c-Fos and Conditioned Taste Aversion

LiCl at doses sufficient to induce conditioned taste aversion (CTA) causes c-Fos expression in the brain regions implicated in CTA formation. It has been reported that nitric oxide (NO) may play a role in CTA learning and LiCl increases both the synthesis and activity of NO synthase (NOS) in the brain. In this study, we examined the effect of central N omega-nitro-L- arginine methyl ester (L-NAME) on the brain c-Fos expression and CTA learning induced by lithium in rats. In the results, intracerebroventricular L-NAME given prior to lithium did not change either the lithium-induced CTA or c-Fos in the relevant brain regions. This suggests that the brain NO system may not be involved in the neuronal activation during lithium-induced CTA formation.

Involvement of dopamine receptors in diethylpropion-induced conditioning place preference

Diethylpropion (DEP) is an amphetamine-like agent used as an anorectic drug. Abuse of DEP has been reported and some restrictions of its use have been recently imposed. The conditioning place preference (CPP) paradigm was used to evaluate the reinforcing properties of DEP in adult male Wistar rats. After initial preferences were determined, animals weighing 250-300 g (N= 7 per group) were conditioned with DEP (10, 15 or 20 mg/kg). Only the dose of 15 mg/kg produced a significant place preference (358 + 39 vs 565 + 48s). Pretreatment with the D1 antagonist SCH 23390 (0.05 mg/kg, sc) 10 min before DEP (15 mg/kg, ip) blocked DEP-induced CPP (418 + 37 vs 389 + 31 s) while haloperidol (0.5 mg/kg, ip), a D2 antagonist, 15 min before DEP was ineffective in modifying place conditioning produced by DEP (385 + 36 vs 536 + 41 s). These results suggest that dopamine D1 receptors mediate the reinforcing effect of DEP.

Eliciting conditioned taste aversion by cobra venom neurotoxin in rats.

An attempt is made to study conditioned taste aversion (CTA) using cobra venom antivenom or lithium chloride as the Unconditioned Stimulus (US). Twenty-four hour water deprived rats were habituated for two consecutive days to drinking tap water in the drinking box for 15 minutes daily. On 3rd day they were allowed to drink 0.1% sodium saccharin. Thirty minutes later, they were injected with cobra venom (45 micrograms), antivenom (0.022 microliter), antivenom followed by venom, lithium chloride (0.15 M, 4% body weight) or physiological saline. After two days of recovery the animals were water deprived for twenty four hours and water intake was measured on the 7th and 8th day. Retention test on the 9th day shows reduced saccharin consumption in the lithium chloride and venom groups. CTA was significantly reduced in the antivenom-venom group and absent in the antivenom and control group. It is concluded cobra venom can induce clear-cut CTA in rats.

Experimental evaluation of the possible neuroleptic activity of clomipramine.

Clomipramine, a new antidepressant, differs from imipramine by having chlorine in position 3 of the aromatic ring and in this respect resembles chlorpromazine. Clomipramine was therefore tested for neuroleptic activity. Clomipramine and imipramine were ineffective in inhibiting the traction response and pinna reflex in mice and in inducing catalepsy in rat. Compared to chlorpromazine they were less potent in blocking conditioned avoidance response and in decreasing spontaneous motor activity and exploratory behaviour. In contrast to chlorpromazine, clomipramine like imipramine was found to enhance methamphetamine-induced stereotyped behaviour. Thus clomipramine like imipramine possesses negligible neuroleptic activity.