Dopaminergic pathway has essential role in excitable behavior, especially fear. Cannabinoids are a class of psychoactive substances and impair memory. The aim of recent study is the effect f dopaminergic pathway in fear memory. In this research, the effect of D1 receptor antagonist Intracerebroventricular injection dopaminergic pathway and Arachidonyl cyclopropyl amide (ACPA) as impair on fear memory, in male mice was studied. One week after surgery of groups, in fear conditioning box, percent freezing and latency to first freezing was recorded. According to tukey test statistical analysis and one-way and two-way phase 5 min and 3 min, percent freezing ACPA dose of 0.1 mg/kg compared to the control group had a significant increase in latency. The percent freezing Dose SCH23390 0.08 mg/site in phase 5 min was significantly reduced in the 3min dose of 0.04 mg/site significant increase in latency indicated. According to Statistical test tow-way and tukey test showed that simultaneous injection of SCH23390 (0.02 mg/mice) and doses of ACPA in phase 3 minutes to 5 minutes and has resulted in a significant reduction in latency and percent freezing. Results indicating that high doses of ACPA cause memory corruption and fear reduction as antagonist SCH23390 infusion D1 cause of the fear.

Introduction: Anxiety is among the most common and treatable mental disorders. Adrenergic and cannabinoid systems have an important role in the neurobiology of anxiety. The elevated plus-maze (EPM) has broadly been used to investigate anxiolytic and anxiogenic compounds. The present study investigated the effects of intraperitoneal (IP) injection of cannabinoid CB1 receptor antagonist (AM251) in the presence of alpha-1 adrenergic antagonist (Prazosin) on rat behavior in the EPM.Methods: In this study, the data were obtained from male Wistar rat, which weighing 200- 250 g. Animal behavior in EPM were videotaped and saved in computer for 10 min after IP injection of saline, AM251 (0.3 mg/kg), Prazosin (0.3 mg/kg) and AM251+Prazosin, subsequently scored for conventional indices of anxiety. During the test period, the number of open and closed arms entries, the percentage of entries into the open arms of the EPM, and the spent time in open and closed arms were recorded. Diazepam was considered as a positive control drug with anxiolytic effect (0.3, 0.6, 1.2 mg/kg).Results: Diazepam increased the number of open arm entries and the percentage of spent time on the open arms. IP injection of AM251 before EPM trial decreased open arms exploration and open arm entry. Whereas, Prazosin increased open arms exploration and open arm entry. This study showed that both substances in simultaneous injection have conflicting effects on the responses of each of these two compounds in a single injection.Discussion: Injection of CB1 receptor antagonist may have an anxiogenic profile in rat, whereas adrenergic antagonist has an anxiolytic effect. Further investigations are essential for better understanding of anxiolytic and anxiogenic properties and neurobiological mechanisms of action and probable interactions of the two systems.

The present study aimed to identify the role of dopaminergic and cannabinoidergic systems in the ghrelininduced hypophagia among meat-type chickens. In the first experiment, intracerebroventricular (ICV) injection was applied to birds with control solution, D1 receptor antagonist (5 nmol), ghrelin (6 nmol), and D1 receptor antagonist plus ghrelin. The second to sixth experiments were similar to the first one, with the difference that D2 receptor antagonist (5 nmol), D3 receptor antagonist (6. 4 nmol), D4 receptor antagonist (6 nmol), the precursor of dopamine (125 nmol), and 6-hydroxy dopamine (150 nmol) instead of D1 antagonist were injected into the broiler chickens. In experiment 7, control solution and different levels of ghrelin antagonists (5, 10, and 20 nmol) were injected. In experiment 8, the chickens were ICV injected with control solution, ghrelin antagonist (10 nmol), dopamine (40 nmol), and ghrelin antagonist plus dopamine. In experiments 9 and 10, CB1 and CB2 receptors antagonist (6. 25μ, g and 5μ, g) were co-injected with ghrelin (6 nmol), respectively, measuring the food intake for 120 min after the injection. It was observed that ghrelin ICV injection considerably reduced food intake, whereas ghrelin antagonist increased food intake, depending on the dose (P<0. 05). In addition, ghrelininduced hypophagia was significantly attenuated by D1 receptor antagonist and 6-hydroxy dopamine (P<0. 05), while the dopamine precursor considerably elevated the ghrelin-induced food intake (P<0. 05). The dopamineinduced feeding behavior was diminished by the co-administration of [D-Lys-3]-GHRP-6 (10 nmol)+dopamine (40 nmol) (P<0. 05). In addition, CB1 receptor antagonists enhanced the ghrelin influence on food intake (P<0. 05). The results implied that the hypophagic impact of ghrelin was probably mediated by D1 and CB1 receptors within neonatal broilers.

Background and purpose: The central nucleus of the amygdala (CeA) is one of the nuclei involved in the reward system. The aim of the current study was to investigate the electrical stimulation (e-stim) effect of the CeA in combination with dopamine D1 receptor antagonist on morphine-induced conditioned place preference (CPP) in male rats. Experimental approach: A 5-day procedure of CPP was used in this study. Morphine was administered at an effective dose of 5 mg/kg, and SCH23390 as a selective D1 receptor antagonist was administrated into the CeA. In addition, the CeA was stimulated with an intensity of the current of 150 μ, A. Finally, the dependence on morphine was evaluated in all experimental groups. Findings /Results: Morphine significantly increased CPP. While the blockade of the D1 receptor of the CeA reduced the acquisition phase of morphine-induced CPP. Moreover, the combination of D1 receptor antagonist and e-stim suppressed morphine-induced CPP, even it induced an aversion. Conclusion and implication: The current study suggests that the administration of dopamine D1 receptor antagonist into the CeA in combination with e-stim could play a prominent role in morphine dependence.