Nicotine improves ethanol-induced memory impairment: The role of dorsal hippocampal NMDA receptors

Rezayof, Ameneh; Shirazi-zand, Zahra; Zarrindast, Mohammad‐Reza; Nayernouri, Touraj

doi:10.1016/j.lfs.2009.12.008

Cited by 29 publications

(23 citation statements)

References 67 publications

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“…At the same time, , the coadministration of an ineffective dose of ethanol with a lower dose of nicotine before retention, significantly reversed the ethanol-induced amnesia and mimicked the effects of pre-test administration of a higher dose of ethanol or nicotine. In support of such findings, we have recently reported that the intra-CA1 (dorsal hippocampal) pre-test injection of nicotine is able to restore ethanol-induced amnesia in mice (5,7,8). Evidence has shown that the amnesic effects of ethanol on both reference and working memory can be blocked by nicotine pretreatment (20).…”

Section: Discussionsupporting

confidence: 52%

“…In addition, according to some later studies, the administration of nicotinic receptor agonists reversed the ethanol-induced amnesia in laboratory animals (7,(18)(19)(20).While nicotine may reverse the ethanol-induced amnesia (similar to pre-test ethanol), the drugs have some opposite effects on other cognitive functions (6,8,21). Where nicotine enhances learning either through a direct effect on attention or affecting the pre-synaptic nicotinic acetylcholine receptors, ethanol may potentially impair learning (4)(5)(6). Taken together, the opposite effects of ethanol and nicotine on cognitive functions (5,8,21) have made the interaction between them complex and hence not fully understood yet.…”

Section: Introductionmentioning

confidence: 96%

“…Both ethanol and nicotine can potentially activate the mesolimbic dopaminergic system projecting from the ventral tegmental area to the nucleus accumbens, hippocampus, amygdala and the prefrontal cortex. These drugs have therefore an important role in reward and rewardrelated learning (3).The impairing effects of ethanol on learning and memory have been well-established in different experimental models (4)(5)(6)including the inhibitory avoidance (7,8), working (9) and spatial memory (10)(11)(12). In agreement with some earlier reports (4,13,14), we noticed that ethanol, when administered both pre-and post-training, can impair inhibitory avoidance memory in a state-dependent manner, and the effect is reversible by pre-test ethanol treatment.…”

Section: Introductionmentioning

confidence: 99%

“…Where nicotine enhances learning either through a direct effect on attention or affecting the pre-synaptic nicotinic acetylcholine receptors, ethanol may potentially impair learning (4)(5)(6). Taken together, the opposite effects of ethanol and nicotine on cognitive functions (5,8,21) have made the interaction between them complex and hence not fully understood yet.…”

Section: Introductionmentioning

confidence: 99%

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Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Raoufi¹,

Moshfegh²,

Piri³

et al. 2016

Journal of Advanced Medical Sciences and Applied Technologies

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The present study investigated the possible involvement of the nucleus accumbens' (NAc) nitric oxide system in nicotine's reversal effect upon ethanol-induced amnesia. The hypothesis was tested through ethanol state-dependent memory assessment in adult male Wistar rats. Bilateral chronic cannulae were implanted in the NAc and the animals were trained in a step-through type inhibitory avoidance memory task. The step-through latency was examined 24 h after animals' training. The pre-training or pre-test intraperitoneal (i.p.) injection of ethanol (0.9 g/kg) decreased the step-through latency, indicating an amnesic effect of the drug. Meanwhile, the pre-test administration of ethanol (0.6 and 0.9 g/kg) could reverse the pre-training ethanol (0.9 g/kg)-induced amnesia, suggesting a state-dependent effect. Similar to ethanol, the pre-test intra-NAc microinjection of nicotine (0.25 and 0.5 µg/rat) alone or nicotine (0.1, 0.25 and 0.5 µg/mouse, intra-NAc) in combination with an ineffective dose of ethanol (0.3 g/kg) could significantly reverse the (pre-training) ethanol-induced memory impairment. The ethanol (0.9 g/kg)-induced amnesia was similarly prevented following the pre-test intra-NAc administration of a nitric oxide synthase (NOS) inhibitor, L-NAME (0.4 and 0.8 µg/rat). Of note, the co-administration of L-NAME (0.04 and 0.08 µg/rat, intra-NAc) with an ineffective dose of nicotine (0.1 µg/rat, intra-NAc) could significantly potentiate the memoryimproving effect of nicotine on ethanol-induced amnesia and resembled the effects of pretest administration of a higher dose of nicotine. Furthermore, while the pre-test intra-NAc injection of L-NAME impaired the memory retrieval by itself, the pre-test intra-NAc administration of L-arginine, a nitric oxide precursor (0.3 and 0.6 µg/rat, intra-NAc), did not exert any effect either alone or in combination with an effective dose of nicotine (0.5 µg/rat, intra-NAc) on pre-training ethanol-induced memory impairment. Our findings indicated a possible role of the nucleus accumbens' nitric oxide system in the improving effects of nicotine on ethanol-induced amnesia and the related state-dependent learning.

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Section: Discussionsupporting

confidence: 52%

Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Raoufi¹,

Moshfegh²,

Piri³

et al. 2016

Journal of Advanced Medical Sciences and Applied Technologies

View full text Add to dashboard Cite

show abstract

“…Interestingly, nicotine can also reverse the amnesic effect of ethanol-induced memory impairment which may lead to the induction of cross STD between ethanol and nicotine [21].…”

Section: Introductionmentioning

confidence: 99%

Alterations in the hippocampal phosphorylated CREB expression in drug state-dependent learning

Alijanpour

Rezayof

Sepehri

et al. 2015

Behavioural Brain Research

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The Impact of the Combined Administration of 1MeTIQ and MK-801 on Cell Viability, Oxidative Stress Markers, and Glutamate Release in the Rat Hippocampus

et al. 2021

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MK-801, as an N-methyl-D-aspartate (NMDA) receptor inhibitor, causes elevation in glutamate release, which may lead to an increase in excitotoxicity, oxidative stress and, consequently, cell death. 1-Methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ) shows antioxidant activity. The aim of the present study was to evaluate the effect of combined treatment with 1MeTIQ and MK-801 on cell viability, antioxidant enzyme activity, and glutamate release in the rat hippocampus. Cytotoxicity was measured using lactate dehydrogenase leakage assay (LDH) and the methyl tetrazolium (MTT) assay; antioxidant enzyme activity (glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), and catalase (CAT)) were measured by ELISA kits. The release of glutamate in the rat hippocampus was measured using in vivo microdialysis methodology. An in vitro study showed that MK-801 induced cell death in a concentration-dependent manner and that 1MeTIQ partially reduced this adverse effect of MK-801. An ex vivo study indicated that MK-801 produced an increase in antioxidant enzyme activity (GPx, GR, and SOD), whereas coadministration of MK-801 and 1MeTIQ restored the activity of these enzymes to the control level. An in vivo microdialysis study demonstrated that combined treatment with both drugs decreased the release of glutamate in the rat hippocampus. The above results revealed that 1MeTIQ shows limited neuroprotective activity under conditions of glutamate-induced neurotoxicity.

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Nicotine improves ethanol-induced memory impairment: The role of dorsal hippocampal NMDA receptors

Cited by 29 publications

References 67 publications

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Alterations in the hippocampal phosphorylated CREB expression in drug state-dependent learning

The Impact of the Combined Administration of 1MeTIQ and MK-801 on Cell Viability, Oxidative Stress Markers, and Glutamate Release in the Rat Hippocampus

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