Enhancement of [3H]dopamine release and its [3H]metabolites in rat striatum by nicotinic drugs

Sakurai, Yasuko; Takáno, Yukio; Kohjimoto, Yoshiro; Honda, Kazuo; Kamiya, Hiro-o

doi:10.1016/0006-8993(82)90499-1

Cited by 87 publications

(27 citation statements)

References 25 publications

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“…Possibly the only evidence that lobeline can activate brain nicotinic AChRs is a report that lobeline-evoked [3H]-dopamine release from mouse striatal synaptosomes is partially mecamylamine-sensitive (Grady et al, 1992). The present experiments, conducted in rats, appear consistent with the suggestion that lobeline releases dopamine from cytosolic stores via a non-nicotinic mechanism (Sakurai et al, 1982). This is not a 'tyramine-like' action, since [3H]-NA release was not enhanced, but rather reduced by an unknown mechanism.…”

Section: Comparisons Between Agonist-evoked [3h]-dopamine and [3h1-nasupporting

confidence: 79%

Untitled

1996

British J Pharmacology

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Section: Comparisons Between Agonist-evoked [3h]-dopamine and [3h1-nasupporting

confidence: 79%

Untitled

1996

British J Pharmacology

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“…DA, dopamine; DOPAC, dihydroxyphenylacetic acid; HVA, homovanillic acid; 5-HIAA, 5-hydroxyindoleacetic acid. Giorguieff-Chesselet et al, 1979;Lehman & Langer, 1982) and synaptosomes (Sakurai et al, 1982;Rapier et al, 1988). It has also been reported that nicotine will stimulate striatal 5-HT release (Westfall et al, 1983).…”

Section: Effect Of Tha On S-ht Reuptakementioning

confidence: 92%

The mechanism of tetrahydroaminoacridine‐evoked release of endogenous 5‐hydroxytryptamine and dopamine from rat brain tissue prisms

Robinson¹,

Souza²,

Cross³

et al. 1989

British J Pharmacology

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1 Tetrahydroaminoacridine (THA) is an acetylcholinesterase (AChE) inhibitor which may have a greater therapeutic effect in Alzheimer-type dementia (ATD) than other cholinergic agents. This suggests possible non-cholinergic properties. We have therefore studied the effects of THA on the release of endogenous 5-hydroxytryptamine (5-HT) from rat cortical prisms and dopamine from striatal prisms. 2 In the presence of K+ (1 mM), THA stimulated release of both 5-HT and dopamine. THA (100pM)-evoked monoamine release was comparable, but not additive with the release produced by K+ (35 mM). The effect was not maximal at 1 mm THA. THA-evoked release of 5-HT was independent of the presence of Ca2 + in the external medium.3 Drugs acting on the cholinergic system, nicotine, mecamylamine, atropine, oxotremorine, physostigmine and neostigmine (all 10pM) had no effect on 5-HT and dopamine release. 4-Aminopyridine (4-AP), a potent acetylcholine-releasing agent, had no effect on 5-HT release and was approximately 100 fold less active than THA on dopamine release. 4 Both THA and reserpine enhanced the release of 5-HT in the presence of the monoamine oxidase inhibitor, pargyline. Reserpine-but not THA-evoked release was abolished in the absence of pargyline. Reserpine (5mg kg -', i.p.) markedly depleted brain monoamine concentrations 3 h after injection, while THA (15 mg kg-1, i.p.) had no effect. 5 Chloroamphetamine and fenfluramine both released 5-HT in a Ca2+-independent manner and with a similar potency to THA, while (+)-amphetamine released dopamine with a similar potency to THA. The effects of the amphetamines were not maximal at 1 mm. However, unlike THA, chloroamphetamine-evoked release of 5-HT was additive with release evoked by K+ (35 mM).6 Clomipramine (IC5o = 0.036upM), imipramine (IC50 = 0.20 pM) and THA (IC50 = 19.9 pM) all inhibited the uptake of [3H]-5-HT into a P2 membrane preparation. However, none of these compounds inhibited [3H]-5-HT uptake into tissue prisms during the release experiments in which the reuptake inhibitor fluoxetine (5puM) was present. 7 We conclude that THA does not release endogenous 5-HT through a cholinergic, reserpine-or amphetamine-like mechanism or through inhibition of reuptake. The possibility exists that the release may occur via blockade of 4-AP-insensitive K+ channels.

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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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Enhancement of [3H]dopamine release and its [3H]metabolites in rat striatum by nicotinic drugs

Cited by 87 publications

References 25 publications

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The mechanism of tetrahydroaminoacridine‐evoked release of endogenous 5‐hydroxytryptamine and dopamine from rat brain tissue prisms

Functional brain imaging of tobacco use and dependence

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