Modulation of ethanol state-dependent learning by dorsal hippocampal NMDA receptors in mice

Rezayof, Ameneh; Sharifi, Khadijeh A.; Zarrindast, Mohammad‐Reza; Rassouli, Yassaman

doi:10.1016/j.alcohol.2008.05.005

Cited by 20 publications

(19 citation statements)

References 60 publications

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“…Duka et al [42] and Nakagawa and Iwasaki [43] reported that ethanol-induced amnesia can be reversed by the administration of the same dose of drug in human and laboratory animals. Previous findings in our laboratory have also indicated that different neurotransmitter systems such as dorsal hippocampal glutamatergic, nitric oxide and dopaminergic systems contribute to ethanol-induced STD [44][45][46]. Signaling pathways triggered with these neurotransmitter systems play an important role in mediating CREBdependent gene expression in neurons [47][48][49].…”

Section: Discussionmentioning

confidence: 80%

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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Section: Discussionmentioning

confidence: 80%

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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“…Nicotine, unlike ethanol enhances learning through a direct effect on attention or through interacting with pre-synaptic nicotinic acetylcholine receptors (nAChR). Nicotine facilitate the release of many neurotransmitters such as acetylcholine, glutamate, dopamine, nor epinephrine, serotonin and γ-amino butyric acid (GABA), all of which are critical to normal learning and memory function [43]. Since ethanol and nicotine have some opposite effects on cognitive functions [44], the interaction between them is complex and not fully understood yet.…”

Section: Discussionmentioning

confidence: 99%

Effects of Melissa officinalis on ethanol state-dependent learning in nicotine- treated mice

Ahmadi¹

2016

MOJAP

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Objectives: Melissa officinalis has antioxidant and antidepressant effects. Besides, it could be good in learning and memory due to its terpenoides. The possible role of Melissa officinalis on ethanol state-dependent learning was studied in adult nicotine-treated male mice.Methods: As a model of memory, a single-trial step-down passive avoidance task was used. In this project, ethanol (0.25, 1 g/kg) and nicotine (0.01, 0.1 mg/ kg) was administrated 30 minutes before training and testing. Melissa officinalis extract (25 mg/kg) was administrated 30 minutes before testing, and then step down latency (SDL) was measured. Key finding:The obtained results showed that administration of ethanol (0.25, 1 g/kg) and nicotine (0.1 mg/ kg) before training could decrease SDL, whereas, nicotine (0.01mg/kg) increased SDL. Conclusion:Pre testing administration of ethanol (1 g/kg), nicotine (0.1 mg/kg) and Melissa officinalis extract (25 mg/kg) could ameliorate decreasing effects of pre training ethanol (0.25, 1 g/kg) and nicotine (0.1 mg/kg) on SDL. Keywords: Mellisa Officinalis Extract (Varangboo); Ethanol State DependentLearning; Nicotine-Treated Mice Institute of Iran, housed in groups of six in stainless-steel cages, and given food and water ad libitum under a standard 12 h light/12 h dark cycle. All training and test sessions were performed in a glass room where only the wooden platform was placed in (standard conditions) middle of the box. Effects of Melissa Officinalis on Ethanol State-Dependent Learning in Nicotine-TreatedFour groups of animals received saline 30 minutes before training and saline, nicotine (0.01, 0.1 mg/kg), ethanol (1, 0.25 g/ kg) and Melissa officinalis extract (25 mg/kg) before testing. Other groups received ethanol( 0.25 g/kg) 30 minutes before training and ethanol (0.25g/kg) before testing, two groups, 30 minutes before training received ethanol (0.25, 1 g/kg) and nicotine (0.1, 0.01 mg/kg). These groups also received saline before testing. Three groups received ethanol (0.25 g/kg), nicotine (0.1 mg/kg) and both of them 30 minutes before training and Melissa officinalis extract (25 mg/kg) before testing. Behavioral proceduresTraining: In the training day, each mice received nicotine or ethanol intra peritoneally (IP) and then 30 min after injection each mice was gently placed on the platform. Five seconds 0.4-mA shock was applied to the grid after which animals were immediately withdrawn from the training apparatus. This training procedure was carried out.Retention test: Twenty-four hours after training, step-down latency was measured 30 min after the last injection. Each mice was gently placed on the platform, without any shock. The stepdown latency (SDL) was taken as a measure of retention. Task:The wood escape platform used for the spatial task at the middle of the glassy box. An electric shock (0.4 mA, 5 s) was delivered to the grid floor by an isolated stimulator. Plant material and extraction procedureThe total plant extract was obtained by extraction of dried and milled plant leaves w...

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“…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: 99%

“…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%

“…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. A considerable body of evidence suggests a solid interaction between ethanol and nicotine in the central nervous system (Collins et al 1993(Collins et al , 1996Smith et al 1999;Lê et al 2003) in which the nicotinic acetylcholine receptors seem to have an important role for such interrelation (3,15,16).Former reports have indicated that the combination of alcohol and nicotine may produce state-dependent learning in humans (17).…”

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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Modulation of ethanol state-dependent learning by dorsal hippocampal NMDA receptors in mice

Cited by 20 publications

References 60 publications

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

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

Effects of Melissa officinalis on ethanol state-dependent learning in nicotine- treated mice

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

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