Stimulation of [<sup>3</sup>H]Dopamine Release by Nicotine in Rat Nucleus Accumbens

Rowell, P.; Carr, Laurence A.; Garner, Ann C.

doi:10.1111/j.1471-4159.1987.tb01013.x

Cited by 140 publications

(49 citation statements)

References 29 publications

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“…Acute exposure to cigarette smoke and nicotine has been found to upregulate dopamine transporter mRNA in the ventral tegmental area (VTA) and substantia nigra (Li et al, 2004), and chronic exposure to cigarette smoke, more so than chronic nicotine alone, has also been found to up-regulate D 1 and D 2 receptor mRNA in the VST (Bahk et al, 2002). Additionally, many in vitro studies of the VST have reported DA release in response to nicotine (Connelly and Littleton, 1983;Marien et al, 1983;Rowell et al, 1987;Sakurai et al, 1982;Westfall et al, 1983).…”

Section: Brain Dopamine Responses To Nicotine and Smokingmentioning

confidence: 99%

Functional brain imaging of tobacco use and dependence

Brody

2006

Journal of Psychiatric Research

176

136

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While most cigarette smokers endorse a desire to quit smoking, only about 14% to 49% will achieve abstinence after 6 months or more of treatment. A greater understanding of the effects of smoking on brain function may (in conjunction with other lines of research) result in improved pharmacological (and behavioral) interventions. Many research groups have examined the effects of acute and chronic nicotine/cigarette exposure on brain activity using functional imaging; the purpose of this paper is to synthesize findings from such studies and present a coherent model of brain function in smokers. Responses to acute administration of nicotine/smoking include: a reduction in global brain activity; activation of the prefrontal cortex, thalamus, and visual system; activation of the thalamus and visual cortex during visual cognitive tasks; and increased dopamine (DA) concentration in the ventral striatum/nucleus accumbens. Responses to chronic nicotine/cigarette exposure include decreased monoamine oxidase (MAO) A and B activity in the basal ganglia and a reduction in α 4 β 2 nicotinic acetylcholine receptor (nAChR) availability in the thalamus and putamen. Taken together, these findings indicate that smoking enhances neurotransmission through cortico-basal ganglia-thalamic circuits either by direct stimulation of nAChRs, indirect stimulation via DA release or MAO inhibition, or a combination of these factors. Activation of this circuitry may be responsible for the effects of smoking seen in tobacco dependent subjects, such as improvements in attentional performance, mood, anxiety, and irritability.

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Section: Brain Dopamine Responses To Nicotine and Smokingmentioning

confidence: 99%

Functional brain imaging of tobacco use and dependence

Brody

2006

Journal of Psychiatric Research

176

136

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“…Activation of nicotinic receptors by nicotine results in an increase in the extracellular concentration of dopamine, which is thought to mediate the rewarding effects of nicotine and maintain tobacco use in dependent individuals (Corrigall et al, 1992;Koob, 1992;Stolerman and Jarvis, 1995). Acute administration of nicotine increases dopamine release from its presynaptic terminals in the striatum in a concentration-dependent manner (Andersson et al, 1981;Dwoskin et al, 1999;Kaiser et al, 1998;Ksir et al, 1995;Pontieri et al, 1996;Rowell et al, 1987;Vezina et al, 1992;Westfall et al, 1983). Synaptic dopamine concentrations are regulated by the dopamine transporter, which transports extracellular dopamine into the presynaptic terminal.…”

Section: Introductionmentioning

confidence: 99%

Nicotine increases dopamine transporter function in rat striatum through a trafficking-independent mechanism

Middleton

Apparsundaram

King-Pospisil

et al. 2007

European Journal of Pharmacology

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In previous in vivo voltammetry studies, acute nicotine administration increased striatal dopamine clearance. The current study aimed to determine whether nicotine also increases [ 3 H]dopamine uptake across the time course of the previous voltammetry studies and whether dopamine transporter trafficking to the cell surface mediates the nicotine-induced augmentation of dopamine clearance in striatum. Rats were administered nicotine (0.32 mg/kg, s.c.); striatal synaptosomes were obtained 5, 10, 40 or 60 min later. Nicotine increased (25%) the V max of [ 3 H]dopamine uptake at 10 and 40 min. To determine whether the increase in V max was due to an increase in dopamine transporter density, [ 3 H]GBR 12935 (1-(2-[bis(4-fluorophenyl)methoxy]ethyl)-4-(3-phenylpropyl)piperazine dihydrochloride) binding was performed using rat striatal membranes; no differences were found between nicotine and saline control groups at 5, 10 or 40 min post-injection, indicating that nicotine did not increase striatal dopamine transporter density; however, [ 3 H]GBR 12935 binding assays determine both cell surface and intracellular dopamine transporter. Changes in cellular dopamine transporter localization in striatum were determined using biotinylation and subfractionation approaches; no differences between nicotine and saline control groups were observed at 10 and 40 min post-injection. These results suggest that the nicotine-induced increase in dopamine uptake and clearance in striatum may occur via a trafficking-independent mechanism.

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“…When stimulated, they increase the neuronal firing rate and transmitter release (Hall & Turner, 1972;Goodman, 1974;Giorguieff et al, 1979;Yoshida et al, 1980;Engberg & Swensson, 1980;Balfour, 1982;Westfall et al, 1983; 1 Author for correspondence. Egan & North, 1986;Rowell et al, 1987;Mereu et al, 1987). Mecamylamine and (sometimes) (+)-tubocurarine are effective blocking agents, suggesting the coexistence of ganglionic and neuromuscular junction subtypes in the same brain area (Morley, 1981;De La Garza et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea‐pigs

Nordberg

Romanelli

Sundwall³

et al. 1989

British J Pharmacology

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1 The effect of acute and chronic (16 days) administration of nicotine on cortical acetylcholine (ACh) release, gross behaviour and brain nicotinic binding sites was investigated in rats and guinea-pigs.2 The drug, injected either subcutaneously (0.45-0.90mgkg-1) or intracerebroventricularly (1, 3 and 5 ig) increased the cortical ACh release, in a dose-dependent manner, through mecamylaminesensitive receptors for 1-2 h in both species. 3 Chronic treatment significantly increased basal ACh release in the rat and slightly lowered it in the guinea-pig, but the response to a challenging dose of nicotine was proportionally maintained in both species. 4 The number of nicotinic receptors was four times higher in the rat than in the guinea-pig and was not dependent on the radioligand used ([3H]-nicotine or [3H]-ACh, in the presence of atropine) to determine this. The nicotinic binding sites showed an apparent increase in chronically treated rats but no change in guinea-pigs. 5 Tolerance to the inhibitory effect of the drug, assessed with the T maze test, was found in the rat. No apparent change in gross behaviour was detected in the guinea-pig. 6 It is concluded that chronic nicotine treatment causes evident tolerance to its inhibitory effect on behaviour in the rat, but no adaptation to its excitatory properties on the cholinergic brain structures in rats and guinea-pigs.

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Stimulation of [³H]Dopamine Release by Nicotine in Rat Nucleus Accumbens

Cited by 140 publications

References 29 publications

Functional brain imaging of tobacco use and dependence

Functional brain imaging of tobacco use and dependence

Nicotine increases dopamine transporter function in rat striatum through a trafficking-independent mechanism

Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea‐pigs

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Stimulation of [3H]Dopamine Release by Nicotine in Rat Nucleus Accumbens

Cited by 140 publications

References 29 publications

Functional brain imaging of tobacco use and dependence

Functional brain imaging of tobacco use and dependence

Nicotine increases dopamine transporter function in rat striatum through a trafficking-independent mechanism

Effect of acute and subchronic nicotine treatment on cortical acetylcholine release and on nicotinic receptors in rats and guinea‐pigs

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Stimulation of [³H]Dopamine Release by Nicotine in Rat Nucleus Accumbens