Possible role of mouse cerebellar nitric oxide in the behavioral interaction between chronic intracerebellar nicotine and acute ethanol administration: Observation of cross-tolerance

Al‐Rejaie, Salim S.; Dar, M. Saeed

doi:10.1016/j.neuroscience.2005.11.034

Cited by 21 publications

(17 citation statements)

References 35 publications

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“…We have provided strong pharmacological evidence that supports a functional relationship between cerebellar nitric oxide and ethanol-induced cerebellar ataxia [1,2]. Ethanol decreases the levels of cerebellar nitrite which were correlated with ethanol-induced cerebellar ataxia [1,2]. The evidence of a strong functional correlation between cerebellar nitric oxide and ethanol-induced cerebellar ataxia is not surprising because, as stated above, NOS is highly expressed in the cerebellum [31].…”

Section: Introductionsupporting

confidence: 65%

“…Nicotine has also been reported to increase soluble cGMP production through activation of NOS, thereby, leading to an increase in the synthesis of nitric oxide [13]. We have provided strong pharmacological evidence that supports a functional relationship between cerebellar nitric oxide and ethanol-induced cerebellar ataxia [1,2]. Ethanol decreases the levels of cerebellar nitrite which were correlated with ethanol-induced cerebellar ataxia [1,2].…”

Section: Introductionsupporting

confidence: 57%

“…Whereas, there is a decline in the extent of cigarette smoking in nonalcoholic population, it has remained consistently high among alcoholics providing strong circumstantial evidence for a functional interaction between alcohol and nicotine [29]. Nicotine markedly attenuates ethanol-induced ataxia via cerebellar nAChRs because it is antagonized by hexamethonium [2]. Ethanol, on the other hand, blocks nicotine-induced memory improvement as well as antagonizes many nicotinic functions within the CNS [24].…”

Section: Introductionmentioning

confidence: 99%

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Involvement of Mouse Cerebellar Neuronal Nitric Oxide Synthase (nNOS) System in the Functional Interaction and Cross-Tolerance between Nicotine and Ethanol

Dar¹

2013

Journal of Drug and Alcohol Research

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Despite cannabinoid and nicotine co‐abuse, no study has examined co‐infused intracerebellar (ICB) THC and nicotine effect on cerebellar ataxia (CA). Aims (i) evaluate ICB THC + nicotine effect on CA; (ii) obtain evidence for nNOS's role in THC‐induced CA, THC – nicotine FA and cross‐tolerance. Methods Rotorod evaluated CA in male CD‐1 mice. All drugs [THC 20μg; nicotine 5ng; nNOS inhibitor (nNOSI; 1,2,5 ng), N’‐nitroguanidine tristrifluracetate] were given by ICB infusion. Results Increased THC‐induced CA by nNOSI indicated nNOS mediation. nNOSI opposed nicotine‐induced attenuation of CA by THC. The antagonism was abolished by 5 ng nNOSI. The response curves of nNOSI + nicotine + THC and aCSF + THC treatments overlapped, further evidence of nNOS mediation. We have previously observed robust cross‐tolerance between nicotine and THC. Results of ongoing chronic study involving nNOSI and nicotine infusion (once daily x 5 days followed 16 h later by acute THC) may further support nNOS role. Discussion Nicotine activates NOS [present in cerebellar neurons except Purkinje cells (PCs)] via release of glutamate. Alleviation of CA is likely due to: increased release of glutamate ►enhanced glutamate transmission ►diffusion of NO into PCs► activation of GC and cGMP production ►low PC firing► removal of CA. Overall, the results support a role of cerebellar nNOS in the nicotine ‐‐THC FA and cross‐tolerance.

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Section: Introductionsupporting
confidence: 65%

Section: Introductionsupporting
confidence: 57%

Section: Introductionmentioning
confidence: 99%

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Involvement of Mouse Cerebellar Neuronal Nitric Oxide Synthase (nNOS) System in the Functional Interaction and Cross-Tolerance between Nicotine and Ethanol
Dar¹
2013
Journal of Drug and Alcohol Research
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Despite cannabinoid and nicotine co‐abuse, no study has examined co‐infused intracerebellar (ICB) THC and nicotine effect on cerebellar ataxia (CA). Aims (i) evaluate ICB THC + nicotine effect on CA; (ii) obtain evidence for nNOS's role in THC‐induced CA, THC – nicotine FA and cross‐tolerance. Methods Rotorod evaluated CA in male CD‐1 mice. All drugs [THC 20μg; nicotine 5ng; nNOS inhibitor (nNOSI; 1,2,5 ng), N’‐nitroguanidine tristrifluracetate] were given by ICB infusion. Results Increased THC‐induced CA by nNOSI indicated nNOS mediation. nNOSI opposed nicotine‐induced attenuation of CA by THC. The antagonism was abolished by 5 ng nNOSI. The response curves of nNOSI + nicotine + THC and aCSF + THC treatments overlapped, further evidence of nNOS mediation. We have previously observed robust cross‐tolerance between nicotine and THC. Results of ongoing chronic study involving nNOSI and nicotine infusion (once daily x 5 days followed 16 h later by acute THC) may further support nNOS role. Discussion Nicotine activates NOS [present in cerebellar neurons except Purkinje cells (PCs)] via release of glutamate. Alleviation of CA is likely due to: increased release of glutamate ►enhanced glutamate transmission ►diffusion of NO into PCs► activation of GC and cGMP production ►low PC firing► removal of CA. Overall, the results support a role of cerebellar nNOS in the nicotine ‐‐THC FA and cross‐tolerance.
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“…There appear to be functionally opposing roles for glutamate N -methyl- d -aspartate and adenosine A 1 receptors (Manzoni et al , 1994), which together may comodulate cerebellar structures important for EtOH-induced motor incoordination (Dar, 2002). Nicotine has been shown to antagonize EtOH-induced motor impairment (Dar et al , 1993, 1994), possibly influenced by nitric oxide (Al-Rejaie and Dar, 2006a) and the cerebellar nitric oxide-guanylyl cyclase messenger system (i.e. cGMP) (Al-Rejaie and Dar, 2006b).…”

Section: Discussionmentioning
confidence: 99%

Motor impairment: a new ethanol withdrawal phenotype in mice
Philibin¹,
Cameron²,
Metten³
et al. 2008
Behavioural Pharmacology
15
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13
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Alcoholism is a complex disorder with genetic and environmental risk factors. The presence of withdrawal symptoms is one criterion for alcohol dependence. Genetic animal models have followed a reductionist approach by quantifying various effects of ethanol withdrawal separately. Different ethanol withdrawal symptoms may have distinct genetic etiologies, and therefore differentiating distinct neurobiological mechanisms related to separate signs of withdrawal would increase our understanding of various aspects of the complex phenotype. This study establishes motor incoordination as a new phenotype of alcohol withdrawal in mice. Mice were made physically dependent on ethanol by exposure to ethanol vapor for 72 h. The effects of ethanol withdrawal in mice from different genetic backgrounds were measured on the accelerating rotarod, a simple motor task. Ethanol withdrawal disrupted accelerating rotarod behavior in mice. The disruptive effects of withdrawal suggest a performance rather than a learning deficit. Inbred strain comparisons suggest genetic differences in magnitude of this withdrawal phenotype. The withdrawal-induced deficits were not correlated with the selection response difference in handling convulsion severity in selectively bred Withdrawal Seizure-Prone and Withdrawal Seizure-Resistant lines. The accelerating rotarod seems to be a simple behavioral measure of ethanol withdrawal that is suitable for comparing genotypes.

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“…Nicotine activates nAChRs in the mesocorticolimbic dopaminergic system that projects from the ventral tegmental area to the nucleus accumbens and the prefrontal cortex [38]. There are also reports indicating that nicotinic and NO systems have interactions [39]. In some other studies, the inhibitory effects of NOS inhibitors on the behavioral effects of nicotine have been shown.…”

mentioning
confidence: 98%

Effects of Melissa officinalis on ethanol state-dependent learning in nicotine- treated mice
Ahmadi¹
2016
MOJAP
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2
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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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Possible role of mouse cerebellar nitric oxide in the behavioral interaction between chronic intracerebellar nicotine and acute ethanol administration: Observation of cross-tolerance

Cited by 21 publications

References 35 publications

Involvement of Mouse Cerebellar Neuronal Nitric Oxide Synthase (nNOS) System in the Functional Interaction and Cross-Tolerance between Nicotine and Ethanol

Involvement of Mouse Cerebellar Neuronal Nitric Oxide Synthase (nNOS) System in the Functional Interaction and Cross-Tolerance between Nicotine and Ethanol

Motor impairment: a new ethanol withdrawal phenotype in mice

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

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