Chronic treatment with ethanol alters the physiological action of nicotine

Majchrzak, Mark J.; Dilsaver, Steven C.

doi:10.1016/0278-5846(92)90013-5

Cited by 9 publications

(5 citation statements)

References 32 publications

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“…This action of ACh at mPFC layer VI pyramidal neurons contributes to the critical role of prefrontal cholinergic signaling to support optimal attention performance in situations requiring high attentional demand (Dalley et al, 2004; Parikh et al, 2007; Bailey et al, 2010; Howe et al, 2010; Guillem et al, 2011). Acute ethanol exposure increases ACh efficacy at α4β2* nAChRs (Aistrup et al, 1999; Cardoso et al, 1999; Zuo et al, 2004), whereas chronic ethanol exposure decreases α4β2* nAChR content (Robles and Sabriá, 2008; Hillmer et al, 2014) and may also decrease nAChR function in vivo (Majchrzak and Dilsaver, 1992). Chronic ethanol exposure during rat development impairs memory and attention in adulthood (Reyes et al, 1989; Nagahara and Handa, 1997; Woolfrey et al, 2005; Brys et al, 2014) and decreases the beneficial effects of nAChR stimulation to augment these mPFC-dependent functions (Nagahara and Handa, 1999).…”

Section: Introductionmentioning

confidence: 99%

Developmental Ethanol Exposure Leads to Long-Term Deficits in Attention and Its Underlying Prefrontal Circuitry

Louth

Bignell

Taylor

et al. 2016

eNeuro

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Chronic prenatal exposure to ethanol can lead to a spectrum of teratogenic outcomes that are classified in humans as fetal alcohol spectrum disorders (FASD). One of the most prevalent and persistent neurocognitive components of FASD is attention deficits, and it is now thought that these attention deficits differ from traditional attention deficit hyperactivity disorder (ADHD) in their quality and response to medication. However, the neuronal mechanisms underlying attention deficits in FASD are not well understood. We show here that after developmental binge-pattern ethanol exposure, adult mice exhibit impaired performance on the five-choice serial reaction time test for visual attention, with lower accuracy during initial training and a higher rate of omissions under challenging conditions of high attention demand. Whole-cell electrophysiology experiments in these same mice find dysregulated pyramidal neurons in layer VI of the medial prefrontal cortex, which are critical for normal attention performance. Layer VI neurons show decreased intrinsic excitability and increased responses to stimulation of both nicotinic acetylcholine receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors. Moreover, although nicotinic acetylcholine responses correlate with performance on the five-choice task in control mice, these relationships are completely disrupted in mice exposed to ethanol during development. These findings demonstrate a novel outcome of developmental binge-pattern ethanol exposure and suggest that persistent alterations to the function of prefrontal layer VI neurons play an important mechanistic role in attention deficits associated with FASD.

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Section: Introductionmentioning

confidence: 99%

Developmental Ethanol Exposure Leads to Long-Term Deficits in Attention and Its Underlying Prefrontal Circuitry

Louth

Bignell

Taylor

et al. 2016

eNeuro

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“…In support of this finding, a study reveals that lesions of the CeA, but not the basolateral amygdala, reduce anxiety-like behaviors and voluntary ethanol consumption in rats (Moller et al ., 1997). Moreover, previous reports established the correlation between ethanol and nicotine (Majchrzak and Dilsaver, 1992; Kokore et al ., 2006) as well as suggested that nAChR is an intermediate site of action for modulation of the nicotine and ethanol effects (Marszalec et al ., 1999). Therefore, the results of the present investigation corroborate well with the notion that nAChR stimulation in CeA might contribute to the ethanol-induced tolerance to the antianxiety effect.…”

Section: Discussionmentioning

confidence: 88%

Neuronal nicotinic acetylcholine receptor of the central amygdala modulates the ethanol-induced tolerance to anxiolysis and withdrawal-induced anxiety in male rats

Duratkar,

Patel,

Jain

2024

Behavioural Pharmacology

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The nicotine acetylcholinergic receptor (nAchR) in the central nucleus of the amygdala (CeA) is known to modulate anxiety traits as well as ethanol-induced behavioral effects. Therefore, the present study investigated the role of CeA nAChR in the tolerance to ethanol anxiolysis and withdrawal-induced anxiety-related effects in rats on elevated plus maze (EPM). To develop ethanol dependence, rats were given free access to an ethanol-containing liquid diet for 10 days. To assess the development of tolerance, separate groups of rats were challenged with ethanol (2 g/kg, i.p.) on days 1, 3, 5, 7 and 10 during the period of ethanol exposure, followed by an EPM assessment. Moreover, expression of ethanol withdrawal was induced after switching ethanol-dependent rats to a liquid diet on day 11, and withdrawal-induced anxiety-like behavior was noted at different post-withdrawal time points using the EPM test. The ethanol-dependent rats were pretreated with intra-CeA (i.CeA) (bilateral) injections of nicotine (0.25 µg/rat) or mecamylamine (MEC) (5 ng/rat) before the challenge dose of ethanol on subthreshold tolerance on the 5th day or on peak tolerance day, that is, 7th or 10th, and before assessment of postwithdrawal anxiety on the 11th day on EPM. Bilateral i.CeA preadministration of nicotine before the challenge dose of ethanol on days 5, 7 and 10 exhibited enhanced tolerance, while injection of MEC, completely mitigated the tolerance to the ethanol-induced antianxiety effect. On the other hand, ethanol-withdrawn rats pretreated i.CeA with nicotine exacerbated while pretreatment with MEC, alleviated the ethanol withdrawal-induced anxiety on all time points. Thus, the present investigation indicates that stimulation of nAChR in CeA negatively modulates the ethanol-induced chronic behavioral effects on anxiety in rats. It is proposed that nAChR antagonists might be useful in the treatment of alcohol use disorder and ethanol withdrawal-related anxiety-like behavior.

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“…Ethanol, on the other hand, blocks nicotine-induced memory improvement as well as antagonizes many nicotinic functions within the CNS [24]. Nicotine antagonizes several physiological functions which are impaired by ethanol [3,21,24,36]. It is plausible that a similar mechanism may be responsible for antagonism by nicotine of ethanol-induced ataxia and sedation in the cerebellum.…”

Section: Introductionmentioning

confidence: 99%

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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Chronic treatment with ethanol alters the physiological action of nicotine

Cited by 9 publications

References 32 publications

Developmental Ethanol Exposure Leads to Long-Term Deficits in Attention and Its Underlying Prefrontal Circuitry

Developmental Ethanol Exposure Leads to Long-Term Deficits in Attention and Its Underlying Prefrontal Circuitry

Neuronal nicotinic acetylcholine receptor of the central amygdala modulates the ethanol-induced tolerance to anxiolysis and withdrawal-induced anxiety in male rats

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

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