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Solati J.,Islamic Azad University at Karaj | Zarrindast M.-R.,Islamic Azad University at Karaj | Zarrindast M.-R.,Tehran University of Medical Sciences | Zarrindast M.-R.,Institute for Studies in Theoretical Physics and Mathematics | Salari A.-A.,Institute for Cognitive Science Studies
Psychiatry and Clinical Neurosciences | Year: 2010

Aims: In the present study, we investigated the possible influence of the opioidergic system of the dorsal hippocampus on anxiety-like behaviors. Methods: Elevated plus-maze, which is one of the methods used for testing anxiety, was used in the present study. Rats were anesthetized with ketamine and xylazine and special cannulas were inserted stereotaxically into the CA1 region of the dorsal hippocampus. After 1 week of recovery, the effects of intra-CA1 administration of morphine (0.25, 0.5, 1 and 2 μg/rat; 1 μl/rat; 0.5 μl/in each side), naloxone (2, 4, 6 and 8 μg/rat), enkephalin (1, 2, 5 and 10 μg/rat) and naltrindole (0.25, 0.5, 1 and 2 μg/rat) on percentage open arm time (%OAT) and percentage open arm entries (%OAE) were determined. Results: Bilateral administration of morphine into CA1 decreases %OAT and %OAE, indicating an anxiogenic-like effect. Intra-CA1 injection of naloxone, an opioid receptor antagonist, increased both %OAT and %OAE, parameters of anxiolytic-like behavior. Bilateral administration of δ-opioid receptor agonist, [D-Pen2,5]-enkephalin acetate hydrate into the CA1, induced an anxiolytic-like effect. Furthermore, intra-CA1 injection of δ-opioid receptor antagonist, naltrindole hydrochloride, increased anxiety-related behaviors. Conclusions: The results of the present study demonstrate that activation of μ-opioid receptors in this area produce an anxiogenic response while activation of δ-opioid receptors produces an anxiolytic response. © 2010 The Authors. Psychiatry and Clinical Neurosciences © 2010 Japanese Society of Psychiatry and Neurology. Source

Burke D.A.,Duke University | Heshmati P.,Institute for Cognitive Science Studies | Kholdebarin E.,Duke University | Levin E.D.,Duke University
European Journal of Pharmacology | Year: 2014

Nicotinic systems have been shown by a variety of studies to be involved in cognitive function. Nicotinic receptors have an inherent property to become desensitized after activation. The relative role of nicotinic receptor activation vs. net receptor inactivation by desensitization in the cognitive effects of nicotinic drugs remains to be fully understood. In these studies, we tested the effects of the α7 nicotinic receptor antagonist methyllycaconitine (MLA), the α4β2 nicotinic receptor antagonist dihydro-β-erythroidine (DHβE), the nonspecific nicotinic channel blocker mecamylamine and the α4β2 nicotinic receptor desensitizing agent sazetidine-A on learning in a repeated acquisition test. Adult female Sprague-Dawley rats were trained on a repeated acquisition learning procedure in an 8-arm radial maze. MLA (1-4 mg/kg), DHβE (1-4 mg/kg), mecamylamine (0.125-0.5 mg/kg) or sazetidine-A (1 and 3 mg/kg) were administered in four different studies either alone or together with the NMDA glutamate antagonist dizocilpine (0.05 and 0.10 mg/kg). MLA significantly counteracted the learning impairment caused by dizocilpine. The overall choice accuracy impairment caused by dizocilpine was significantly attenuated by co-administration of DHβE. Low doses of the non-specific nicotinic antagonist mecamylamine also reduced dizocilpine-induced repeated acquisition impairment. Sazetidine-A reversed the accuracy impairment caused by dizocilpine. These studies provide evidence that a net decrease in nicotinic receptor activity can improve learning by attenuating learning impairment induced by NMDA glutamate blockade. This adds to evidence in cognitive tests that nicotinic antagonists can improve cognitive function. Further research characterizing the efficacy and mechanisms underlying nicotinic antagonist and desensitization induced cognitive improvement is warranted. © 2014 Elsevier B.V. Source

Zarrindast M.R.,Tehran University of Medical Sciences | Zarrindast M.R.,Institute for Research in Fundamental Sciences | Zarrindast M.R.,Institute for Cognitive Science Studies | Piri M.,Islamic Azad University at Ardabil | And 2 more authors.
Pharmacology Biochemistry and Behavior | Year: 2012

In the present study, the possible effect of nitric oxide agents injected into the nucleus accumbens (NAc) in the presence or absence of nicotine on morphine state-dependent memory in adult male Wistar rats was investigated. As a model of memory, a step-through type inhibitory avoidance task was used. Post-training injection of morphine (4 and 6 mg/kg) dose dependently induced the impairment of memory retention. Administration of morphine (4 and 6 mg/kg) before retention induced state-dependent retrieval of the memory acquired under post-training morphine (6 mg/kg) influence. Injection of nicotine before retention (0.25 and 0.5 mg/kg) alone and nicotine (0.1, 0.25 and 0.5 mg/kg) plus an ineffective dose of morphine (2 mg/kg) reversed the post-training morphine-induced memory impairment. The amnesia elicited by morphine (6 mg/kg) was also prevented by pre-retention intra-NAc administration of a nitric oxide synthase (NOS) inhibitor, l-NAME (0.24 μg/rat, intra-NAc). Interestingly, an ineffective dose of nicotine (0.1 mg/kg) in combination with low doses of l-NAME (0.06 and 0.12 μg/rat, intra-NAc) synergistically improved memory performance impaired by morphine given after training. It is important to note that intra-NAc administration of l-NAME before retention impaired memory retrieval by itself. In contrast, pre-retention administration of l-arginine, a nitric oxide (NO) precursor (0.25 and 0.5 μg/rat, intra-NAc), which had no effect alone, prevented the nicotine reversal of morphine effect on memory. The results suggest a possible role for nitric oxide of nucleus accumbens in the improving effect of nicotine on the morphine-induced amnesia and morphine state-dependent memory. © 2011 Elsevier Inc. Source

Zarrindast M.R.,Tehran University of Medical Sciences | Zarrindast M.R.,Institute for Studies in Fundamental science IPM | Zarrindast M.R.,Institute for Cognitive Science Studies | Mahboobi S.,Tehran University of Medical Sciences | And 2 more authors.
Journal of Psychopharmacology | Year: 2011

In the present study the influence of the dopaminergic system(s) of the amygdala on the anxiolytic-like effect of the cannabinoid CB1 receptor agonist, arachydonilcyclopropylamide (ACPA), in male Wistar rats was investigated. An elevated plus-maze test of anxiety was used to assess anxiety-like behaviors. The results showed that bilateral intra-amygdala injections of ACPA (0.125, 1.25 and 5 ng/rat) and the mixed dopamine D1/D2 receptor agonist, apomorphine, at different doses (0.001, 0.01 and 0.1 μg/rat) increased percentage open arm time (%OAT) and percentage open arm entries (%OAE), indicating an anxiolytic-like effect for both of the drugs. In contrast, intra-amygdala administration of the dopamine D1 receptor antagonist SCH23390 (0.5 and 1 μg/rat) and the dopamine D2 receptor antagonist, sulpiride (2 and 3 μg/rat) decreased %OAT and %OAE, suggesting an anxiogenic-like effect for both of the drugs. Interestingly, pretreatment with a sub-effective dose of apomorphine (0.0005 μg/rat) increased, while SCH23390 (0.25 μg/rat) and sulpiride (1.5 μg/rat) decreased the anxiolytic-like effect of ACPA. It can be concluded that the dopaminergic system of the amygdala may be involved, at least partly, in the anxiolytic-like effects induced by ACPA in the rat amygdala. © 2011 The Author(s). Source

Sardari M.,University of Tehran | Rezayof A.,University of Tehran | Khodagholi F.,Shahid Beheshti University of Medical Sciences | Zarrindast M.-R.,Tehran University of Medical Sciences | And 2 more authors.
International Journal of Neuropsychopharmacology | Year: 2014

The present study was designed to investigate the involvement of GABA-A receptors of the basolateral amygdala (BLA) in the impairing effect of acute stress on memory retrieval. The BLAs of adult male Wistar rats were bilaterally cannulated and memory retrieval was measured in a step-through type passive avoidance apparatus. Acute stress was evoked by placing the animals on an elevated platform for 10, 20 and 30 min. The results indicated that exposure to 20 and 30 min stress, but not 10 min, before memory retrieval testing (pre-test exposure to stress) decreased the step-through latency, indicating stress-induced memory retrieval impairment. Intra-BLA microinjection of a GABA-A receptor agonist, muscimol (0.005-0.02 μg/rat), 5 min before exposure to an ineffective stress (10 min exposure to stress) induced memory retrieval impairment. It is important to note that pre-test intra-BLA microinjection of the same doses of muscimol had no effect on memory retrieval in the rats unexposed to 10 min stress. The blockade of GABA-A receptors of the BLA by injecting an antagonist, bicuculline (0.4-0.5 μg/rat), 5 min before 20 min exposure to stress, prevented stress-induced memory retrieval. Pre-test intra-BLA microinjection of the same doses of bicuculline (0.4-0.5 μg/rat) in rats unexposed to 20 min stress had no effect on memory retrieval. In addition, pre-treatment with bicuculline (0.1-0.4 μg/rat, intra-BLA) reversed muscimol (0.02 μg/rat, intra-BLA)-induced potentiation on the effect of stress in passive avoidance learning. It can be concluded that pre-test exposure to stress can induce memory retrieval impairment and the BLA GABA-A receptors may be involved in stress-induced memory retrieval impairment. © CINP 2013. Source

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