The sensitizing effect of acute nicotine on amphetamine-stimulated behavior and dopamine efflux requires activation of β2 subunit-containing nicotinic acetylcholine receptors and glutamate N-methyl-d-aspartate receptors

Kim, Myung N.; Jutkiewicz, Emily M.; Zhang, Minjia; Gnegy, Margaret E.

doi:10.1016/j.neuropharm.2010.10.003

Cited by 16 publications

(15 citation statements)

References 66 publications

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“…In the experiments using nACh receptor antagonists, a subtype non-selective nACh antagonist, MEC (1 mg/kg), a specific α7 nACh antagonist, MLA (10 mg/kg), a specific α4β2 nACh antagonist, DHβE (5 mg/kg) or saline (vehicle) was intraperitoneally injected 15 min before the nicotine treatment. The dosage of nACh antagonists was set to a level that sufficiently antagonized the respective nACh receptors in previous studies [MEC: ( Gomita et al, 1989 ), DHβE: ( Blondel et al, 2000 ), and MLA: ( Blondel et al, 2000 ; Kim et al, 2011 ; Liu, 2014 )].…”

Section: Methodsmentioning

confidence: 99%

Nicotine Elicits Convulsive Seizures by Activating Amygdalar Neurons

et al. 2017

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Nicotinic acetylcholine (nACh) receptors are implicated in the pathogenesis of epileptic disorders; however, the mechanisms of nACh receptors in seizure generation remain unknown. Here, we performed behavioral and immunohistochemical studies in mice and rats to clarify the mechanisms underlying nicotine-induced seizures. Treatment of animals with nicotine (1–4 mg/kg, i.p.) produced motor excitement in a dose-dependent manner and elicited convulsive seizures at 3 and 4 mg/kg. The nicotine-induced seizures were abolished by a subtype non-selective nACh antagonist, mecamylamine (MEC). An α7 nACh antagonist, methyllycaconitine, also significantly inhibited nicotine-induced seizures whereas an α4β2 nACh antagonist, dihydro-β-erythroidine, affected only weakly. Topographical analysis of Fos protein expression, a biological marker of neural excitation, revealed that a convulsive dose (4 mg/kg) of nicotine region-specifically activated neurons in the piriform cortex, amygdala, medial habenula, paratenial thalamus, anterior hypothalamus and solitary nucleus among 48 brain regions examined, and this was also suppressed by MEC. In addition, electric lesioning of the amygdala, but not the piriform cortex, medial habenula and thalamus, specifically inhibited nicotine-induced seizures. Furthermore, microinjection of nicotine (100 and 300 μg/side) into the amygdala elicited convulsive seizures in a dose-related manner. The present results suggest that nicotine elicits convulsive seizures by activating amygdalar neurons mainly via α7 nACh receptors.

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Section: Methodsmentioning

confidence: 99%

Nicotine Elicits Convulsive Seizures by Activating Amygdalar Neurons

et al. 2017

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“…Associated psychostimulant-induced increases in dopamine neurotransmission are also altered by nicotine. Indeed, combinations of nicotine and cocaine or amphetamine have additive or synergistic effects on dopamine release in the nucleus accumbens (174–176). Cocaine and amphetamines also interact strongly with the cholinergic system.…”

Section: Concurrent Use Of Nicotine and Psychostimulantsmentioning

confidence: 99%

Mechanisms and genetic factors underlying co-use of nicotine and alcohol or other drugs of abuse

Cross

Lotfipour

Leslie

2016

The American Journal of Drug and Alcohol Abuse

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Concurrent use of tobacco and alcohol or psychostimulants represents a major public health concern, with use of one substance influencing consumption of the other. Co-abuse of these drugs leads to substantial negative health outcomes, reduced cessation, and high economic costs, but the underlying mechanisms are poorly understood. Epidemiological data suggest that tobacco use during adolescence plays a particularly significant role. Adolescence is a sensitive period of development marked by major neurobiological maturation of brain regions critical for reward processing, learning and memory, and executive function. Nicotine exposure during this time produces a unique and long-lasting vulnerability to subsequent substance use, likely via actions at cholinergic, dopaminergic, and serotonergic systems. In this review, we discuss recent clinical and preclinical data examining the genetic factors and mechanisms underlying co-use of nicotine and alcohol or cocaine and amphetamines. We evaluate the critical role of nicotinic acetylcholine receptors throughout, and emphasize the dearth of preclinical studies assessing concurrent drug exposure. We stress important age and sex differences in drug responses, and highlight a brief, low-dose nicotine exposure paradigm that may better model early use of tobacco products. The escalating use of e-cigarettes among youth necessitates a closer look at the consequences of early adolescent nicotine exposure on subsequent alcohol and drug abuse.

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“…These doses were chosen based on previous reports Kim et al, 2011). We administered MDMA at a 5 mg/Kg dose because, although it is relatively low, it induces robust behavioral activation (Ball et al, 2009).…”

Section: Drug Treatmentmentioning

confidence: 99%

Heteromeric nicotinic receptors are involved in the sensitization and addictive properties of MDMA in mice

Ciudad-Roberts¹,

Camarasa²,

Piccoli³

et al. 2013

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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We have investigated the effect of nicotinic receptor ligands in the behavioral sensitization (hyperlocomotion) and rewarding properties (conditioned place preference paradigm, CPP) of 3,4-methylenedioxy-methamphetamine (MDMA) in mice. Each animal received intraperitoneal pretreatment with either saline, dihydro-E-erythroidine (DHEE, 1 mg/Kg) or varenicline (VAR, 0.3 mg/Kg), 15 min prior to subcutaneous saline or MDMA (5 mg/Kg), for 10 consecutive days. On day 1, both DHEE and VAR inhibited the MDMA-induced hyperlocomotion. After 10 days of treatment, MDMA induced a hyperlocomotion that was not reduced (rather enhanced) in antagonistpretreated animals. This early hyperlocomotion was accompanied by a significant increase in heteromeric nicotinic receptors in cortex that was not blocked by DHEE or VAR. Behavioral sensitization to MDMA was highest 2 weeks after the discontinuation of MDMA treatment. This additional increase in sensitivity was prevented in animals pretreated with DHEE or VAR. At this time, MDMA-treated mice showed a significant increase in heteromeric receptors in cortex that was prevented by DHEE and VAR. An involvement of α7 nicotinic receptors in this effect is ruled out.MDMA (10 mg/Kg) induced positive CPP that was abolished by DHEE (2 mg/Kg) and VAR (2 mg/Kg). Moreover, chronic nicotine pretreatment (2 mg/Kg, ip, b.i.d., for 14 days) caused MDMA, administered at a low dose (3 mg/kg), to induce CPP, which would otherwise not occur. Finally, present results point out that heteromeric nicotinic receptors are involved in locomotor sensitization and addictive potential induced by MDMA. Thus, varenicline might be a useful drug to treat both tobacco and MDMA abuse at once.

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The sensitizing effect of acute nicotine on amphetamine-stimulated behavior and dopamine efflux requires activation of β2 subunit-containing nicotinic acetylcholine receptors and glutamate N-methyl-d-aspartate receptors

Cited by 16 publications

References 66 publications

Nicotine Elicits Convulsive Seizures by Activating Amygdalar Neurons

Nicotine Elicits Convulsive Seizures by Activating Amygdalar Neurons

Mechanisms and genetic factors underlying co-use of nicotine and alcohol or other drugs of abuse

Heteromeric nicotinic receptors are involved in the sensitization and addictive properties of MDMA in mice

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