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Publications (2)5.18 Total impact

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    ABSTRACT: Experimental results indicate a mutual interaction between cannabinoidergic and GABAergic systems; however, the interaction between these systems on corticosterone release has not been fully investigated. In this study, we treated male mice with either cannabinoid compounds alone or in combination with diazepam. Blood samples were collected at 60 min post-injection. The serum corticosterone (CORT) level was measured using ELISA technique. Acute treatment of mice by cannabinoid receptor agonist WIN55212-2 (2.5 mg/kg; i.p.) resulted in a significant reduction of CORT, while treatment with either endocannabinoid reuptake inhibitor AM404 or endocannabinoid degradation enzyme inhibitor URB597 increased CORT compared to control group. Co-administration of AM404 or URB597 with cannabinoid CB1 receptor antagonist AM251 blocked the effect of these compounds on CORT. Treatment of mice with different doses of diazepam alone did not alter CORT compared to control group. However, co-administration of diazepam and either AM404 or WIN55212-2 significantly reduced CORT compared to the respective group treated with cannabinoid compound alone. Co-administration of ineffective dose of URB597 and ineffective dose of diazepam increased CORT level compared to groups treated with each compound alone. In conclusion, our findings suggest that the endogenous cannabinoid system is active as a modulator of CORT in mice and diazepam can alter the effect of cannabinoid system in the modulation of neuroendocrine functions.
    Neurochemical Research 08/2009; 35(1):60-6. · 2.13 Impact Factor
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    ABSTRACT: Several studies have shown that cannabinoids have anticonvulsant properties that are mediated through activation of the cannabinoid CB1 receptors. In addition, endogenous cannabinoid compounds (endocannabinoids) regulate synaptic transmission and dampen seizure activity via activation of the same receptors. The aim of this study was to evaluate the possible interactions between antiepileptic effects of cannabinoid compounds and diazepam using electroshock-induced model of seizure in mice. Electroconvulsions were produced by means of an alternating current (ear-clip electrodes, fixed current intensity 35 mA, stimulus duration 0.2 s) and tonic hindlimb extension was taken as the endpoint. All experiments were performed on groups of ten mice and the number of animals who did not display seizure reported as percent protection. Intraperitoneal (i.p.) administration of diazepam (0.25-2 mg/kg) and CB1 receptor agonist WIN55212-2 (0.5-4 mg/kg) dose dependently produced an antiepileptic effect evaluated in terms of increased percentage of protection against electroshock-induced seizure. Logistic regression analysis indicated synergistic interactions in anticonvulsant action after co-administration of diazepam and WIN55212-2 in fixed-ratio combination of 3:1 (diazepam:WIN55212-2), while an additive effect was resulted after co-administration of 1:1 and 1:3 fixed-ratio combinations. Administration of various doses of the endocannabinoid reuptake inhibitor, AM404, did not produce any effect on electroshock-induced seizure. Moreover, co-administration of AM404 and diazepam did not produce significant interaction in antiepileptic properties of these compounds. Administration of the fatty acid amide hydrolase inhibitor, URB597, produced significant antiepileptic effect. Co-administration of URB597 and diazepam led to an antagonistic interaction in protection against shock-induced seizure. Co-administration of different doses of the cannabinoid CB1 receptor antagonist, AM251 did not alter the antiepileptic effect of diazepam in the electroshock-induced seizure test. These results demonstrate that endocannabinoid system participates in the modulation of seizure and combination of small doses of exogenous CB1 receptor agonists with diazepam may have effective consequences in seizure control. Furthermore, inhibiting the endocannabinoid degradation could be more efficacious in modulating seizure than preventing their uptake. This study also suggests that the effects of cannabinoids on epilepsy depend on the relative cannabinoid responsiveness of GABAergic and glutamatergic neurotransmission. While, the antiepileptic effects of cannabinoid compounds are likely by affecting excitatory glutamate neurotransmission, the antagonistic interaction between cannabinoid compounds and diazepam to protect seizure is due to the cannabinoid action on inhibitory GABAergic system.
    Journal of Neural Transmission 07/2008; 115(11):1501-11. · 3.05 Impact Factor