Chronic nicotine modifies the effects of morphine on extracellular striatal dopamine and ventral tegmental GABA

• Published in: Journal of neurochemistry Vol. 107; no. 3; pp. 844 - 854
• Main Authors: Vihavainen, Tanja, Relander, Toni R.A, Leiviskä, Riikka, Airavaara, Mikko, Tuominen, Raimo K, Ahtee, Liisa, Piepponen, Timo Petteri
• Format: Journal Article
• Language: English
• Published: Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01.11.2008; Blackwell Publishing Ltd; Blackwell
• Subjects: 3,4-dyhydroxylphenylalanine; 3-hydroxybenzylhydrazine dihydrochloride; Animals; Anticonvulsants. Antiepileptics. Antiparkinson agents; Biochemistry; Biological and medical sciences; Brain - drug effects; Brain - metabolism; caudate putamen; Central nervous system; Central neurotransmission. Neuromudulation. Pathways and receptors; chronic oral nicotine treatment; Dihydroxyphenylalanine - metabolism; dopamine; Dopamine - metabolism; Extracellular Fluid - metabolism; Fundamental and applied biological sciences. Psychology; GABA; gamma-Aminobutyric Acid - drug effects; gamma-Aminobutyric Acid - metabolism; Homovanillic Acid - metabolism; Hydroxyindoleacetic Acid - metabolism; Male; Medical sciences; Mice; Microdialysis; morphine; Morphine - pharmacology; Motor Activity - drug effects; Narcotics; Narcotics - pharmacology; Neurology; Neuropharmacology; Neurotransmitter Agents - metabolism; Neurotransmitters; Nicotine; Nicotine - pharmacology; Nicotinic Agonists - pharmacology; nipecotic acid; nucleus accumbens; Pharmacology. Drug treatments; Rodents; substantia nigra; Time; ventral tegmental area; Vertebrates: nervous system and sense organs; α-methyltyrosine; 3,4-dyhydroxylphenylalanine; 3-hydroxybenzyl- hydrazine dihydrochloride; Central nervous system; Morphine; nipecotic acid; Encephalon; Caudate nucleus; Ventral tegmental area; α-methyltyrosine; Release; substantia nigra; Dopamine; Interaction; caudate putamen; Rodentia; chronic oral nicotine treatment; Basal ganglion; Corpus striatum; nucleus accumbens; Catecholamine; Extracellular; Vertebrata; Chronic; Mammalia; Treatment; Mouse; microdialysis; Neurotransmitter; GABA; Nicotine
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1111/j.1471-4159.2008.05676.x

Previously, we have shown that 7-week oral nicotine treatment enhances morphine-induced behaviors and dopaminergic activity in the mouse brain. In this study, we further characterized the nicotine-morphine interaction in the mesolimbic and nigrostriatal dopaminergic systems, as well as in the GABAergic control of these systems. In nicotine-pretreated mice, morphine-induced dopamine release in the caudate putamen and nucleus accumbens was significantly augmented, as measured by microdialysis. Chronic nicotine treatment did not change basal extracellular concentrations of dopamine and its metabolites in the caudate putamen and nucleus accumbens, nor did it affect the rate of dopamine synthesis, as assessed by 3-hydroxybenzylhydrazine dihydrochloride-induced DOPA accumulation. GABAergic control of dopaminergic activity was studied by measuring extracellular GABA in the presence of nipecotic acid, an inhibitor of GABA uptake. Acute (0.3 mg/kg or 0.5 mg/kg i.p.) and chronic nicotine, as well as morphine (15 mg/kg s.c.) in control mice decreased nipecotic acid-induced increase in extracellular GABA in the ventral tegmental area/substantia nigra (VTA/SN). In contrast, in nicotine-treated mice, morphine increased GABA levels in the presence of nipecotic acid. We did not find any alterations in GABAB-receptor function after chronic nicotine treatment. Thus, our data show that chronic nicotine treatment sensitizes dopaminergic systems to morphine and affects GABAergic systems in the VTA/SN.