Effect of nicotine on extracellular levels of neurotransmitters assessed by microdialysis in various brain regions: Role of glutamic acid

Tóth, Eugene; Sershen, Henry; Hashim, Audrey; Vízi, E. S.; Lajtha, Ábel

doi:10.1007/bf00966669

Cited by 180 publications

(125 citation statements)

References 26 publications

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“…Nicotine anxiogenic-like responses could be mediated by the release of some neurotransmitters, such as glutamate and noradrenaline (Brazell et al 1991;Toth et al 1992;Sharp and Matta 1993;Fu et al 1998) which are known to facilitate stress/anxiety-related behaviour (Gray et al 1994;Guimaraes et al 1991;Jessa et al 1995;Onaka et al 1996). The stimulatory effects of nicotine on corticotrophin releasing factor and ACTH release (Okuda et al 1993;Bremner et al 1996;Herman and Cullinan 1997) Anxiety and emotional disorders seem to be an important factor for the establishment and maintenance of tobacco addiction (Pomerleau, 1986).…”

Section: Previous Studies Have Reported Behavioural Interactions Betwmentioning

confidence: 99%

Role of the cannabinoid system in the effects induced by nicotine on anxiety-like behaviour in mice

2006

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Rationale: Acute behavioural effects and motivational responses induced by nicotine can be modulated by the endocannabinoid system supporting the existence of a physiological interaction between these two systems. Objectives: The present study was designed to examine the possible involvement of the cannabinoid system in the anxiolytic-and anxiogenic-like responses induced by nicotine in mice. Methods:

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Section: Previous Studies Have Reported Behavioural Interactions Betwmentioning

confidence: 99%

Role of the cannabinoid system in the effects induced by nicotine on anxiety-like behaviour in mice

2006

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“…It is well documented that nicotine stimulates dopamine (DA) release in the nucleus accumbens and striatum (Imperato et al, 1986;Damsma et al, 1989;Toth et al, 1992;Benwell and Balfour, 1994;Nisell et al, 1994a;Pontieri et al, 1996;Mirza et al, 1996;Marshall et al, 1997). This property has been related to the addictive and behavioral properties of nicotine (Benwell and Balfour, 1992;Corrigall et al, 1992;Di Chiara and Imperato, 1988).…”

Section: Introductionmentioning

confidence: 99%

Effect of Ginseng Saponins on Enhanced Dopaminergic Transmission and Locomotor Hyperactivity Induced by Nicotine

Kim

Shim

Chung

et al. 2005

Neuropsychopharmacol

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Several studies have shown that behavioral hyperactivity induced by psychomotor stimulants is prevented by ginseng saponins. In an attempt to investigate whether the effect of ginseng saponins is through their inhibitory action on the enhanced dopaminergic transmission by psychomotor stimulants, we examined the effects of ginseng total saponin (GTS) presynaptically on nicotine-induced dopamine (DA) release in the striatum of freely moving rats using in vivo microdialysis technique and postsynaptically on the in vitro and in vivo binding of [ 3 H]raclopride to DA D 2 receptors. Also, we examined the effects of GTS on nicotine-induced locomotor hyperactivity and on nicotine-induced Fos protein expression in the nucleus accumbens and striatum. Systemic pretreatment with GTS (100 and 400 mg/kg, intraperitoneally (i.p.)) resulted in a dose-dependent inhibition of locomotor hyperactivity induced by nicotine. GTS decreased nicotine-induced DA release in the striatum in a dose-dependent manner. However, GTS had no effects on resting levels of locomotor activity and extracellular DA in the striatum. GTS inhibited the in vitro binding of [ 3 H]raclopride to rat striatal membranes with an IC 50 of 5.1471.09 mM. High doses of GTS (400 and 800 mg/kg, i.p.) resulted in decreases in the in vivo binding of [ 3 H]raclopride in the striatum. GTS decreased nicotine-induced Fos protein expression in the nucleus accumbens and striatum, reflecting the inhibition by GTS of nicotine-induced enhancement of dopaminergic transmission. The results of the present study suggest that GTS acts not only on dopaminergic neurons directly or indirectly to prevent nicotine-induced DA release but also postsynaptically by binding to DA D 2 receptors. This may explain the blocking effect of GTS on behavioral activation induced by nicotine and conceivably by other psychostimulants. Our data raise the possibility that GTS, by attenuating nicotine-induced enhancement of dopaminergic transmission, may prove to be a useful therapeutic agent for nicotine addiction and warrant further investigation on its effect on nicotine's rewarding property.

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“…All of these studies evaluated the effects of systemic nicotine injection on dopamine release in the rat nucleus accumbens using in vivo microdialysis and all of these studies showed that inhibiting nAChRs expressed on cell bodies, or blocking action potentials with tetrodotoxin, resulted in virtual elimination of nicotine-induced dopamine release in the accumbens. Other studies that evaluated the effects of nicotine infused into dopaminergic nerve terminals (acumbens, striatum, frontal cortex) resulted in readily detected increases in dopamine release [115,116]. These contradictory findings might be explained by the more recent observation that used cyclic voltametry to obtain a better resolution of time-dependent effects of nicotine application on dopamine release.…”

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confidence: 99%

The subtypes of nicotinic acetylcholine receptors on dopaminergic terminals of mouse striatum

Grady

Salminen

Laverty

et al. 2007

Biochemical Pharmacology

229

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This review summarizes studies that attempted to determine the subtypes of nicotinic acetylcholine receptors (nAChR) expressed in the dopaminergic nerve terminals in the mouse. A variety of experimental approaches has been necessary to reach current knowledge of these subtypes, including in situ hybridization, agonist and antagonist binding, function measured by neurotransmitter release from synaptosomal preparations, and immunoprecipitation by selective antibodies. Early developments that facilitated this effort include the radioactive labeling of selective binding agents, such as [ 125 I]-α-bungarotoxin and [ 3 H]-nicotine, advances in cloning the subunits, and expression and evaluation of function of combinations of subunits in Xenopus oocytes. The discovery of epibatidine and α-conotoxin MII (α-CtxMII), and the development of nAChR subunit null mutant mice have been invaluable in determining which nAChR subunits are important for expression and function in mice, as well as allowing validation of the specificity of subunit specific antibodies. These approaches have identified five nAChR subtypes of nAChR that are expressed on dopaminergic nerve terminals. Three of these contain the α6 subunit (α4α6β2β3, α6β2β3, α6β2) and bind α-CtxMII with high affinity. One of these three subtypes (α4α6β2β3) also has the highest sensitivity to nicotine of any native nAChR that has been studied, to date. The two subtypes that do not have high affinity for α-CtxMII (α4β2, α4α5β2) are somewhat more numerous than the α6* subtypes, but do bind nicotine with high affinity. Given that our first studies detected readily measured differences in sensitivity to agonists and antagonists among these five nAChR subtypes, it seems likely that subtype selective compounds could be developed that would allow therapeutic manipulation of diverse nAChRs that have been implicated in a number of human conditions. Alterations in nicotinic cholinergic receptor (nAChRs) number or function have been implicated in psychopathologies such as anxiety, attention deficit hyperactivity disorder, depression, schizophrenia (reviewed in [1,2,3]), at least one form of familial epilepsy [4], and Parkinson's and Alzheimer's diseases [5]. It is not particularly surprising that nAChRs might play important roles in modulating several human diseases given that binding sites for nicotinic ligands such as [ 125 I]-α-bungarotoxin [6,7,8], [ 3 H]-nicotine [7,8] Corresponding author: Sharon R Grady e-mail: sharon.grady@colorado.edu phone: 303-492-9677 fax: 303-492-8063 mailing address: Institute for Behavioral Genetics University of Colorado 447UCB Boulder, CO 80309. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered w...

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Effect of nicotine on extracellular levels of neurotransmitters assessed by microdialysis in various brain regions: Role of glutamic acid

Cited by 180 publications

References 26 publications

Role of the cannabinoid system in the effects induced by nicotine on anxiety-like behaviour in mice

Role of the cannabinoid system in the effects induced by nicotine on anxiety-like behaviour in mice

Effect of Ginseng Saponins on Enhanced Dopaminergic Transmission and Locomotor Hyperactivity Induced by Nicotine

The subtypes of nicotinic acetylcholine receptors on dopaminergic terminals of mouse striatum

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