Nicotine and alcohol: the role of midbrain dopaminergic neurons in drug reinforcement

Morel, Carole; Montgomery, Sarah; Han, Ming–Hu

doi:10.1111/ejn.14160

Cited by 29 publications

(31 citation statements)

References 380 publications

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“…Like cocaine and opioids, DA release has been heavily implicated in the reinforcing effects of alcohol [68–70]. Though the precise mechanisms remain poorly understood, there is evidence suggesting that alcohol increases DA neurotransmission by increasing the activity of VTA DA neurons [68,71–73]. Interestingly, while this increased activity of VTA DA neurons in response to alcohol leads to large DA release in the NAc, the NAc shell exhibits larger transient increases in DA compared to the core, consistent with other drugs of abuse [30,32,59,60].…”

Section: Medial Vta‐mnacsh Da Release and Sudsmentioning

confidence: 81%

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Roles of dopamine and glutamate co‐release in the nucleus accumbens in mediating the actions of drugs of abuse

et al. 2020

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Projections of ventral tegmental area dopamine (DA) neurons to the medial shell of the nucleus accumbens have been increasingly implicated as integral to the behavioral and physiological changes involved in the development of substance use disorders (SUDs). Recently, many of these nucleus accumbens-projecting DA neurons were found to also release the neurotransmitter glutamate. This glutamate co-release from DA neurons is critical in mediating the effect of drugs of abuse on addiction-related behaviors. Potential mechanisms underlying the role(s) of dopamine/glutamate co-release in contributing to SUDs are unclear. Nevertheless, an important clue may relate to glutamate's ability to potentiate loading of DA into synaptic vesicles within terminals in the nucleus accumbens in response to drug-induced elevations in neuronal activity, enabling a more robust release of DA after stimulation. Here, we summarize how drugs of abuse, particularly cocaine, opioids, and alcohol, alter DA release in the nucleus accumbens medial shell, examine the potential role of DA/glutamate co-release in mediating these effects, and discuss future directions for further investigating these mechanisms.

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Section: Medial Vta‐mnacsh Da Release and Sudsmentioning

confidence: 81%

Section: Medial Vta‐mnacsh Da Release and Sudsmentioning

confidence: 99%

Roles of dopamine and glutamate co‐release in the nucleus accumbens in mediating the actions of drugs of abuse

et al. 2020

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“…Importantly, the high‐affinity α4β2 is most densely expressed on dopaminergic VTA neurons while the α7‐homomeric nAChRs are primarily located on excitatory glutamatergic terminals that synapse on dopamine neurons. Both of which have been demonstrated to increase dopamine signaling via activation by EtOH and/or NIC (reviewed in Morel et al ). Evidence suggests that EtOH may potentiate the actions of most nAChRs while inhibiting nicotine‐induced receptor desensitization (Aistrup et al ; Marszalec et al ).…”

Section: Discussionmentioning

confidence: 99%

Co‐administration of ethanol and nicotine heightens sensitivity to ethanol reward within the nucleus accumbens (NAc) shell and increasing NAc shell BDNF is sufficient to enhance ethanol reward in naïve Wistar rats

Waeiss

Knight

Engleman

et al. 2019

Journal of Neurochemistry

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Alcohol use disorder most commonly presents as a polydrug disorder where greater than 85% are estimated to smoke. EtOH and nicotine (NIC) co‐abuse or exposure results in unique neuroadaptations that are linked to behaviors that promote drug use. The current experiments aimed to identify neuroadaptations within the mesolimbic pathway produced by concurrent EtOH and NIC exposure. The experiments used four overall groups of male Wistar rats consisting of vehicle, EtOH or NIC alone, and EtOH+NIC. Drug exposure through direct infusion into the posterior ventral tegmental area (pVTA) stimulated release of glutamate and dopamine in the nucleus accumbens (NAc) shell, which was quantified through high‐performance liquid chromatography. Additionally, brain‐derived neurotrophic factor (BDNF) protein levels were measured via enzyme‐linked immunosorbent assay (ELISA). A second experiment investigated the effects of drug pretreatment within the pVTA on the reinforcing properties of EtOH within the NAc shell through intracranial self‐administration (ICSA). The concluding experiment evaluated the effect of NAc shell pretreatment with BDNF on EtOH reward utilizing ICSA within that region. The data indicated that only EtOH+NIC administration into the pVTA simultaneously increased glutamate, dopamine, and BDNF in the NAc shell. Moreover, only pVTA pretreatment with EtOH+NIC enhanced the reinforcing properties of EtOH in the NAc shell. BDNF pretreatment in the NAc shell was also sufficient to enhance the reinforcing properties of EtOH in the NAc shell. The collected data suggest that concurrent EtOH+NIC exposure results in a distinct neurochemical response and neuroadaptations within the mesolimbic pathway that alter EtOH reward.

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“…The dopamine transmission from the VTA into the nucleus accumbens regulates the rewarding system and involves addiction behaviour 29 and anxiety behaviour. 8 Previous report suggested that ethanol actions in the VTA increase in the rewarding responses. Chronic ethanol intoxication produces opposite effects of acute ethanol intoxication and/or compensatory/homeostatic effects on the expression, localisation, and function of proteins.…”

Section: Resultsmentioning

confidence: 98%

Thunbergia laurifolia Linn. Extract Protects Ethanol Addiction and Increases Dopamine Synthesis

2021

TJNPR

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Ethanol consumption is a widespread problem throughout the world. Ethanol mainly acts on dopaminergic system which is a major circuit in mediating the reward system of ethanol and other drugs leading to the change in behaviour. 1,2 Dopaminergic neurons in the ventral tegmental area (VTA) innervates several brain areas including the nucleus accumbens affected by acute and chronic ethanol exposure. Ethanol was shown to cause excitation of dopaminergic neurons in the VTA in vitro and in vivo. 3 The enhancement of the firing rate of the VTA dopaminergic neurons correlates with dopamine release and tyrosine hydroxylase of the VTA and nucleus accumbens. 4,5 On the other hand, chronic ethanol administration decreases the VTA dopaminergic neurons firing rate and activity. 6,7 The dopaminergic connection between the VTA and nucleus accumbens is associated with a critical role in addiction and anxiety-like behaviours. 8,9 Ethanol addicted rodents spent more time in the non-preference compartment of the conditioned place preference (CPP) behaviour model after chronic ethanol administration. 10,11 The changes of synaptic output induced by chronic ethanol administration

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Nicotine and alcohol: the role of midbrain dopaminergic neurons in drug reinforcement

Cited by 29 publications

References 380 publications

Roles of dopamine and glutamate co‐release in the nucleus accumbens in mediating the actions of drugs of abuse

Roles of dopamine and glutamate co‐release in the nucleus accumbens in mediating the actions of drugs of abuse

Co‐administration of ethanol and nicotine heightens sensitivity to ethanol reward within the nucleus accumbens (NAc) shell and increasing NAc shell BDNF is sufficient to enhance ethanol reward in naïve Wistar rats

Thunbergia laurifolia Linn. Extract Protects Ethanol Addiction and Increases Dopamine Synthesis

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