Nitric oxide in the nucleus accumbens is involved in retrieval of inhibitory avoidance memory by nicotine.

Department of Neuroscience, School of Advanced Medical Technologies, Tehran University of Medical Sciences, Tehran, Iran.
Pharmacology Biochemistry and Behavior (Impact Factor: 2.82). 11/2011; 101(1):166-73. DOI: 10.1016/j.pbb.2011.11.010
Source: PubMed

ABSTRACT 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 6mg/kg) dose dependently induced the impairment of memory retention. Administration of morphine (4 and 6mg/kg) before retention induced state-dependent retrieval of the memory acquired under post-training morphine (6mg/kg) influence. Injection of nicotine before retention (0.25 and 0.5mg/kg) alone and nicotine (0.1, 0.25 and 0.5mg/kg) plus an ineffective dose of morphine (2mg/kg) reversed the post-training morphine-induced memory impairment. The amnesia elicited by morphine (6mg/kg) was also prevented by pre-retention intra-NAc administration of a nitric oxide synthase (NOS) inhibitor, l-NAME (0.24μg/rat, intra-NAc). Interestingly, an ineffective dose of nicotine (0.1mg/kg) in combination with low doses of l-NAME (0.06 and 0.12μg/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 0.5μg/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.

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    ABSTRACT: Interactions between cannabinoid and glutamate systems have been demonstrated in some brain areas associated with mnemonic functions. This study investigates the effects of bilateral post-training intra-nucleus accumbens (NAc) shell administrations of glutamate NMDA receptor agents on memory impairment induced by cannabinoid CB1 receptor activation during a step-through inhibitory avoidance (IA) task. Our results showed post-training administration of ACPA (CB1 receptor agonist; 3ng/side) impairs IA memory consolidation, whereas AM251 (CB1 receptor antagonist; 0.3, 3 and 30ng/side), NMDA (0.3, 3 and 30ng/side), and D-AP7 (NMDA receptor antagonist; 3, 30 and 300ng/side) were ineffective. However, co-administration of AM251 (30ng/side) or NMDA (30ng/side) with ACPA (3ng/side) prevented the memory-impairing effect of ACPA. Meanwhile, co-administration of NMDA (30ng/side) and a subthreshold dose of ACPA (0.15ng/side) decreased memory consolidation. Moreover, post-training microinjection of AM251 (30ng/side) or D-AP7 (300ng/side) prevented memory impairment induced by co-administration of subthreshold doses of NMDA and ACPA. The data indicated that NMDA receptor mechanism(s), at least partly, play(s) a role in modulating the effect of ACPA on memory consolidation in the NAc shell.
    Behavioural brain research 04/2014; · 3.22 Impact Factor
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    ABSTRACT: In the present study, the effects of intra-dorsal hippocampal (intra-CA1) injections of nitric oxide (NO) agents on muscimol state-dependent memory were examined in mice. A single-trial step-down passive avoidance task was used for the assessment of memory retrieval in adult male NMRI mice. Post-training intra-CA1 administration of a GABAA receptor agonist, muscimol (0.05 and 0.1μg/mouse) dose dependently induced impairment of memory retention. Pre-test injection of muscimol (0.05 and 0.1μg/mouse) induced state-dependent retrieval of the memory acquired under post-training muscimol (0.1μg/mouse, intra-CA1) influence. Pre-test injection of a NO precursor, L-arginine (1 and 2μg/mouse, intra-CA1) improved memory retention, although the low dose of the drug (0.5μg/mouse) did not affect memory retention. Pre-test injection of an inhibitor of NO-synthase, L-NAME (0.5 and 1μg/mouse, intra-CA1) impaired memory retention, although the low dose of the drug (0.25μg/mouse) did not affect memory retention. In other series of experiments, pre-test intra-CA1 injection of L-arginine (0.25 and 0.5μg/mouse) 5min before the administration of muscimol (0.1μg/mouse, intra-CA1) dose dependently inhibited muscimol state-dependent memory. Pre-test intra-CA1 administration of L-arginine (0.125, 0.25 and 0.5μg/mouse) by itself cannot affect memory retention. Pre-test intra-CA1 injection of L-NAME (0.25μg/mouse, intra-CA1) reversed the memory impairment induced by post-training administration of muscimol (0.1μg/mouse, intra-CA1). Moreover, pre-test administration of L-NAME (0.125 and 0.25μg/mouse, intra-CA1) with an ineffective dose of muscimol (0.025μg/mouse, intra-CA1) significantly restored the retrieval and induced muscimol state-dependent memory. Pre-test intra-CA1 administration of L-NAME (0.0625, 0.125 and 0.25μg/mouse) by itself cannot affect memory retention. It may be suggested that the nitric oxide in the dorsal hippocampal area play an important role in muscimol state-dependent memory.
    Pharmacology Biochemistry and Behavior 12/2013; · 2.82 Impact Factor


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