ArticleJournal of neurochemistry2014
Enhanced synthesis and release of dopamine in transgenic mice with gain-of-function α6* nAChRs.
Article in Journal of neurochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Expression of sensitized β2 nAChR subunits in VTA neurons enhances intravenous nicotine self-administration in male rats.Neuropharmacology · 2024Article
- Role of α6-Nicotinic Receptors in Alcohol-Induced GABAergic Synaptic Transmission and Plasticity to Cholinergic Interneurons in the Nucleus Accumbens.Molecular neurobiology · 2023Article
- β2 nAChR Activation on VTA DA Neurons Is Sufficient for Nicotine Reinforcement in Rats.eNeuro · 2023Article
- Lipid metabolism in dopaminergic neurons influences light entrainment.Journal of neurochemistry · 2023Article
- Paraquat exposure produces sex-dependent reduction in binge-like alcohol drinking in high alcohol-preferring mice.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2023Article
- Nicotinic acetylcholine receptors: Conventional and unconventional ligands and signaling.Neuropharmacology · 2020Review
- Nicotine and alcohol: the role of midbrain dopaminergic neurons in drug reinforcement.The European journal of neuroscience · 2019Review
- Genetic correlations between nicotine reinforcement-related behaviors and propensity toward high or low alcohol preference in two replicate mouse lines.Genes, brain, and behavior · 2019Article
- Alterations in the nigrostriatal dopamine system after acute systemic PhIP exposure.Toxicology letters · 2018Article
- Article
- The Nicotinic α6-Subunit Selective Antagonist bPiDI Reduces Alcohol Self-Administration in Alcohol-Preferring Rats.Neurochemical research · 2016Article
- Crucial roles of the CHRNB3-CHRNA6 gene cluster on chromosome 8 in nicotine dependence: update and subjects for future research.Translational psychiatry · 2016Review
- Neural and behavioural changes in male periadolescent mice after prolonged nicotine-MDMA treatment.Metabolic brain disease · 2016Article
- r-bPiDI, an α6β2* Nicotinic Receptor Antagonist, Decreases Nicotine-Evoked Dopamine Release and Nicotine Reinforcement.Neurochemical research · 2015Article
- α6-Containing nicotinic acetylcholine receptors in midbrain dopamine neurons are poised to govern dopamine-mediated behaviors and synaptic plasticity.Neuroscience · 2015Article
- Evidence for a role for α6(∗) nAChRs in l-dopa-induced dyskinesias using Parkinsonian α6(∗) nAChR gain-of-function mice.Neuroscience · 2015Article
- The nicotinic α6 subunit gene determines variability in chronic pain sensitivity via cross-inhibition of P2X2/3 receptors.Science translational medicine · 2015Article
- Behavioral, neurochemical, and pathologic alterations in bacterial artificial chromosome transgenic G2019S leucine-rich repeated kinase 2 rats.Neurobiology of aging · 2015Article
- Subacute manganese exposure in rats is a neurochemical model of early manganese toxicity.Neurotoxicology · 2014Article
- The role of the habenula in drug addiction.Frontiers in human neuroscience · 2014Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
α6β2* nicotinic acetylcholine receptors (nAChRs)s in the ventral tegmental area to nucleus accumbens (NAc) pathway are implicated in the response to nicotine, and recent work suggests these receptors play a role in the rewarding action of ethanol. Here, we studied mice expressing gain-of-function α6β2* nAChRs (α6L9'S mice) that are hypersensitive to nicotine and endogenous acetylcholine. Evoked extracellular dopamine (DA) levels were enhanced in α6L9'S NAc slices compared to control, non-transgenic (non-Tg) slices. Extracellular DA levels in both non-Tg and α6L9'S slices were further enhanced in the presence of GBR12909, suggesting intact DA transporter function in both mouse strains. Ongoing α6β2* nAChR activation by acetylcholine plays a role in enhancing DA levels, as α-conotoxin MII completely abolished evoked DA release in α6L9'S slices and decreased spontaneous DA release from striatal synaptosomes. In HPLC experiments, α6L9'S NAc tissue contained significantly more DA, 3,4-dihydroxyphenylacetic acid, and homovanillic acid compared to non-Tg NAc tissue. Serotonin (5-HT), 5-hydroxyindoleacetic acid, and norepinephrine (NE) were unchanged in α6L9'S compared to non-Tg tissue. Western blot analysis revealed increased tyrosine hydroxylase expression in α6L9'S NAc. Overall, these results show that enhanced α6β2* nAChR activity in NAc can stimulate DA production and lead to increased extracellular DA levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.