Interactions between low concentrations of ethanol and nicotine on firing rate of ventral tegmental dopamine neurones

Clark, Abigail M.; Little, H.J.

doi:10.1016/j.drugalcdep.2004.03.001

Cited by 37 publications

(27 citation statements)

References 34 publications

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“…For individuals with co-occurring disorders, those who also had an opiate use disorder were significantly less likely to achieve smoking cessation (as compared to those with an alcohol use disorder) but for all groups length of smoking cessation treatment was predictive of greater smoking cessation. First, studies have shown the synergistic effect between nicotine and other substances, which may promote dual use and subsequently hinder efforts at smoking cessation (Clark & Little, 2004;Gerasimov et al, 2000;Liu et al, 2011;Tizabi, Bai, Copeland, & Taylor, 2007). Although our findings are attenuated by small sample size, we believe this may have important implications for individuals with opiate addictions, given that such individuals tend to have very poor smoking cessation outcomes (Okoli et al, 2010).…”

Section: Journal Of Dual Diagnosismentioning

confidence: 46%

Smoking Cessation Outcomes and Predictors Among Individuals With Co-occurring Substance Use and/or Psychiatric Disorders

Okoli

Khara

2014

Journal of Dual Diagnosis

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Section: Journal Of Dual Diagnosismentioning

confidence: 46%

Smoking Cessation Outcomes and Predictors Among Individuals With Co-occurring Substance Use and/or Psychiatric Disorders

Okoli

Khara

2014

Journal of Dual Diagnosis

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“…For example, Bloom and Siggins (1987) described regionally distinct effects of ethanol on cell firing ranging from increased firing to depression when recording from inferior olive, hippocampal, cerebellar, and locus coeruleus neurons. In accord with this observation, Givens and Breese (1990a) showed that systemic administration of ethanol depressed neural activity in the medial septum, but not the lateral septum, whereas others described ethanol increases in firing rate of neurons in the ventral tegmental area (Brodie et al, 1990;Clark and Little, 2004). Mereu and Gessa (1985) found that low doses of systemically administered ethanol inhibited firing of neurons in the substantia nigra reticulataFan effect enhanced by muscimol and eliminated by bicuculline.…”

Section: Regional Specificity Of Ethanol On Functions Altered By Gabamentioning

confidence: 90%

A Conceptualization of Integrated Actions of Ethanol Contributing to its GABAmimetic Profile: A Commentary

Criswell

Breese

2005

Neuropsychopharmacol

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Early behavioral investigations supported the contention that systemic ethanol displays a GABAmimetic profile. Microinjection of GABA agonists into brain and in vivo electrophysiological studies implicated a regionally specific action of ethanol on GABA function. While selectivity of ethanol to enhance the effect of GABA was initially attributed an effect on type-1-benzodiazepine (BZD)-GABA A receptors, a lack of ethanol's effect on GABA responsiveness from isolated neurons with this receptor subtype discounted this contention. Nonetheless, subsequent work identified GABA A receptor subtypes, with limited distribution in brain, sensitive to enhancement of GABA at relevant ethanol concentrations. In view of these data, it is hypothesized that the GABAmimetic profile for ethanol is due to activation of mechanisms associated with GABA function, distinct from a direct action on the majority of postsynaptic GABA A receptors. The primary action proposed to account for ethanol's regional specificity on GABA transmission is its ability to release GABA from some, but not all, presynaptic GABAergic terminals. As systemic administration of ethanol increases neuroactive steroids, which can enhance GABA responsiveness, this elevated level of neurosteroids is proposed to magnify the effect of GABA released by ethanol. Additional factors contributing to the degree to which ethanol interacts with GABA function include an involvement of GABA B and other receptors that influence ethanol-induced GABA release, an effect of phosphorylation on GABA responsiveness, and a regional reduction of glutamatergic tone. Thus, an integration of these consequences induced by ethanol is proposed to provide a logical basis for its in vivo GABAmimetic profile.

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“…Thus, a differential action of drugs upon these release events may contribute to differences in their addictive properties. Studies have reported that acute ethanol can increase spontaneous VTA-DA neuron firing by a direct excitatory action (Brodie et al, 1990(Brodie et al, , 1999Clark and Little, 2004). Ethanol has also been shown to reduce the activity of VTA GABAergic neurons (Gallegos et al, 1999;Stobbs et al, 2004), suggesting ethanol could also enhance spontaneous activity by reducing inhibitory tone.…”

Section: Effects Of Acute and Chronic Ethanol On Vta-da Neuronal Actimentioning

confidence: 94%

Glutamate‐Dopamine Cotransmission and Reward Processing in Addiction

Lapish

Seamans

Chandler

2006

Alcoholism Clin & Exp Res

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While Dale's principle of "one neuron, one neurotransmitter" has undergone revisions to incorporate evidence of the corelease of atypical neurotransmitters such as neuropeptides, the corelease of classical neurotransmitters has only recently been realized. Surprisingly, numerous studies now indicate that the corelease of neurotransmitters in the mammalian central nervous system is not an obscure and rare phenomenon but is widespread and involves most classical neurotransmitters systems. However, the suggestion that glutamate can be coreleased with dopamine (DA) has remained controversial. Furthermore, glutamate-DA cotransmission has not yet been seriously considered in the context of the neurocircuitry of addiction. If glutamate is in fact coreleased with DA as some evidence now suggests, this may have significant implications for advancing our understanding of the interactive role that these 2 neurotransmitters play in cognitive and reward processes. In this commentary, we review the evidence for and against glutamate as a cotransmitter and discuss the potential role of glutamate-DA corelease in addiction. In particular, we describe a recently proposed model in which coreleased glutamate transmits a temporally precise prediction error signal of reward described by Schultz et al., whereas the function of coreleased DA is to exert prolonged modulatory influences on neuronal activity. In addition, we suggest that as alcohol consumption transitions from recreational use to addiction, there is a corresponding transition in the reward valence signal from better than predicted to worse than predicted.

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Interactions between low concentrations of ethanol and nicotine on firing rate of ventral tegmental dopamine neurones

Cited by 37 publications

References 34 publications

Smoking Cessation Outcomes and Predictors Among Individuals With Co-occurring Substance Use and/or Psychiatric Disorders

Smoking Cessation Outcomes and Predictors Among Individuals With Co-occurring Substance Use and/or Psychiatric Disorders

A Conceptualization of Integrated Actions of Ethanol Contributing to its GABAmimetic Profile: A Commentary

Glutamate‐Dopamine Cotransmission and Reward Processing in Addiction

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