ArticleThe Journal of pharmacology and experimental therapeutics2009
Nicotinic receptor activation increases [3H]dopamine uptake and cell surface expression of dopamine transporters in rat prefrontal cortex.
Article in The Journal of pharmacology and experimental therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Exploring the Relationship Between VMAT2 and DAT Expression, Psychotic Experiences, Craving, and Treatment Motivation in Male Patients with Methamphetamine Use Disorder.Journal of clinical medicine · 2024Article
- Dopamine Transporter, PhosphoSerine129 α-Synuclein and α-Synuclein Levels in Aged LRRK2 G2019S Knock-In and Knock-Out Mice.Biomedicines · 2022Article
- [The Journal of pharmacology and experimental therapeutics · 2020Article
- Salicylate-Induced Ototoxicity of Spiral Ganglion Neurons: CaNeurotoxicity research · 2019Article
- Molecular Mechanism and Dynamics ofACS omega · 2017Article
- Allosteric modulatory effects of SRI-20041 and SRI-30827 on cocaine and HIV-1 Tat protein binding to human dopamine transporter.Scientific reports · 2017Article
- Age-dependent dopamine transporter dysfunction and Serine129 phospho-α-synuclein overload in G2019S LRRK2 mice.Acta neuropathologica communications · 2017Article
- Gene expression profiling of midbrain dopamine neurons upon gestational nicotine exposure.Medical & biological engineering & computing · 2017Article
- HIV-1 transgenic rats display an increase in [(3)H]dopamine uptake in the prefrontal cortex and striatum.Journal of neurovirology · 2016Article
- Pharmacogenetics of nicotine addiction: role of dopamine.Pharmacogenomics · 2014Review
- Dysregulation of kappa-opioid receptor systems by chronic nicotine modulate the nicotine withdrawal syndrome in an age-dependent manner.Psychopharmacology · 2012Article
- HIV-1 Tat protein decreases dopamine transporter cell surface expression and vesicular monoamine transporter-2 function in rat striatal synaptosomes.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Article
- Effect of environmental enrichment on methylphenidate-induced locomotion and dopamine transporter dynamics.Behavioural brain research · 2011Article
- Methylphenidate treatment in adolescent rats with an attention deficit/hyperactivity disorder phenotype: cocaine addiction vulnerability and dopamine transporter function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011Article
- Upregulation of norepinephrine transporter function by prolonged exposure to nicotine in cultured bovine adrenal medullary cells.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Previous research shows that nicotine increases dopamine (DA) clearance in rat prefrontal cortex (PFC) and striatum via a nicotinic receptor (nAChR)-mediated mechanism. The present study investigated whether activation of nAChRs regulates DA transporter (DAT) function through a trafficking-dependent mechanism. After nicotine administration (0, 0.3, and 0.8 mg/kg s.c., 15-1440 min after injection), DAT function and trafficking in synaptosomes of PFC and striatum were determined. nAChR mediation of the effect of nicotine on DAT function and trafficking in PFC was determined by pretreatment with mecamylamine, dihydro-beta-erythroidine, or methyllycaconitine. Nicotine (0.8 mg/kg, 15 and 30 min after injection) increased the maximal velocity (V(max)) of [3H]DA uptake in PFC with no change in K(m), compared with control. Biotinylation and Western blot assays showed that nicotine (0.8 mg/kg; 30 min) increased DAT cell surface expression in PFC. In contrast, a lower dose of nicotine (0.3 mg/kg; 30 min) did not alter DAT function and trafficking in PFC. Pretreatment with mecamylamine, dihydro-beta-erythroidine, or methyllycaconitine (1.5, 8.0, and 10.0 mg/kg s.c., respectively) completely blocked the nicotine-induced increase in V(max) in PFC. In addition, mecamylamine completely blocked the nicotine-induced increase in DAT cell surface expression in PFC. Nicotine did not increase DAT function and cell surface expression in striatum, indicating that nicotine modulates DAT function in a brain region-specific manner. Thus, results from the present study suggest that the nicotine-induced increases in DAT function and cell surface expression in PFC may mediate some of the behavioral effects of nicotine.
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