Nicotine induced c-fos expression in the striatum is mediated mostly by dopamine D1 receptor and is dependent on NMDA stimulation

Kiba, Hideo; Angayarkanni, Jayaraman

doi:10.1016/0169-328x(94)90205-4

Cited by 81 publications

(56 citation statements)

References 58 publications

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“…Acute nicotine elevates Fos expression in various brain regions, including dopaminergic target areas (Ren and Sagar, 1992;Matta et al, 1993;Pang et al, 1993;Kiba and Jayaraman, 1994;Panagis et al, 1996;Salminen et al, 1996;Valentine et al, 1996). In the present study, GTS decreased nicotine-induced Fos protein expression in the nucleus accumbens and striatum.…”

Section: Discussionsupporting

confidence: 61%

“…This reflects the inhibition of nicotine-induced enhancement of dopaminergic transmission by GTS. From our results, the effect of GTS may be due in large measure to its inhibitory effect on DA release because DA D 1 receptor, but not D 2 receptor, mediates nicotine-induced Fos expression in the striatum and nucleus accumbens (Kiba and Jayaraman, 1994;Nisell et al, 1997;Svenningsson and Le Moine, 2002). In addition, GTS may exert an inhibitory effect on DA D 1 receptors, which should be investigated by further studies.…”

Section: Discussionmentioning

confidence: 71%

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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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Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 71%

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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“…The present finding that nicotine challenge does not significantly affect FLI in the STR of drug-naive animals contrasts the results of Kiba and Jayaraman (1994). These authors found that acute injections of nicotine, in doses similar to those used in the present study, induced FLI in the STR, mainly in its central and dorsomedial parts, although no statistical analysis appears to have been performed.…”

Section: Discussioncontrasting

confidence: 56%

“…Furthermore, the expression of c-fos and other immediate early genes has been found to be increased in DA target areas by several drugs that increase the extracellular concentration of DA, such as cocaine, amphetamine, and morphine (Graybiel et al 1990;Young et al 1991;Moratalla et al 1993;Liu et al 1994). Indeed, systemic administration of nicotine has also been shown to increase Fos-like immunoreactivity (FLI) in several brain regions, including some which receive their dopaminergic innervation from the ventral tegmental area (VTA) (Ren and Sagar 1992; Matta et al Pang et al 1993;Kiba and Jayaraman 1994). Moreover, local administration of nicotine into the VTA of drug-naive rats has recently been shown to increase FLI in the NAC .…”

mentioning

confidence: 99%

Chronic Nicotine Enhances Basal and Nicotine-Induced Fos Immunoreactivity Preferentially in the Medial Prefrontal Cortex of the Rat

Nisell

Nomikos

Chergui

et al. 1997

Neuropsychopharmacology

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In the present study, expression of the immediate early gene protein products Fos and Jun-B within the dorsolateral striatum, the core and shell of the nucleus accumbens (NAC), the medial prefrontal cortex (mPFC), and the ventrolateral orbital cortex was examined. Rats were injected SC with either saline or nicotine (0.5 mg/kg) once daily for 12 days. On day 13, animals received a challenge injection of either saline or nicotine (0.5 or 1.0 mg/kg, SC) and 2 h later their brains were examined for Fos-like (FLI) and Jun-B-like (JLI) immunoreactivity. Chronic nicotine significantly increased basal expression of FLI selectively in the mPFC. Nicotine challenge significantly increased FLI in the mPFC of saline-treated animals and even further increased FLI in the mPFC of nicotine-treated animals. In the shell of the NAC, nicotine challenge also increased FLI in nicotine-treated animals, whereas it increased JLI only in saline-treated animals. After chronic nicotine treatment, injection of D 1 receptor antagonist SCH 23390 (0.1 mg/kg, IP) 10 min before a nicotine challenge (0.5 mg/kg, SC), significantly attenuated the nicotine-induced FLI in theThe rewarding and dependence-producing actions of nicotine appear to be due, at least in part, to stimulation of the mesolimbic dopamine (DA) system (see Grenhoff and Svensson 1989; Clark 1990;Svensson et al. 1990;Corrigall 1991;Nisell et al. 1995). Thus, nicotinic receptors have been found to be located on both the cell bodies and the terminals of mesolimbic DA neurons Schwartz et al. 1984), and lesions of the mesolimbic DA system attenuate nicotine selfadministration and nicotine-induced locomotor stimulation in rats (Clarke et al. 1988; Corrigall et al. 1992). Furthermore, nicotine has been shown to increase neuronal activity, particularly burst activity, of midbrain DA cells Grenhoff et al. 1986;Lichtensteiger et al. 1982;Mereu et al. 1987. Systemically administered nicotine also increases release (Imperato et al. 1986;Nisell et al. 1994), synthesis, and metabolism of DA (Andersson et al. 1981;Grenhoff and Svensson 1988) The nicotine-induced locomotion is significantly enhanced with chronic pretreatment with the drug (Morrison and Stephenson 1972;Clarke and Kumar 1983;Benwell and Balfour 1992;Nisell et al. 1996). Although this behavioral activation is to a considerable extent dependent on mesolimbic dopaminergic transmission (see above), previous reports utilizing in vivo microdialysis have demonstrated not only increased (Benwell and Balfour 1992) but also unchanged (Damsma et al. 1989;Nisell et al. 1996) nicotine-induced DA release in the NAC after chronic nicotine treatment. Moreover, the behavioral sensitization observed after chronic, intermittent nicotine treatment for 12 days has been shown to be parallelled by an increase in nicotine-induced DA release in the medial prefrontal cortex (mPFC), whereas the response in the NAC was unaffected . Recently, by means of in vivo voltammetry, systemic administration of nicotine was shown to increase DA release to a greater ext...

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“…above). In addition, the postsynaptic consequences, as reflected by an activation of immediate-early genes, of the enhanced DA overflow in the NAC following systemically administered nicotine (Kiba and Jayaraman 1994) can be mimicked by nicotine application into the VTA . However, the putative role of nAChRs in the VTA in the above described behavioral and biochemical manifestations of the nicotine withdrawal syndrome has, as yet, not been investigated.…”

mentioning

confidence: 99%

Behavioral and Biochemical Manifestations of Mecamylamine-Precipitated Nicotine Withdrawal in the Rat Role of Nicotinic Receptors in the Ventral Tegmental Area

Hildebrand

Panagis

Svensson

et al. 1999

Neuropsychopharmacology

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Brain mesolimbic dopamine (DA) neurons are considered critical for the dependence-producing action of nicotine, and its stimulatory effect on behavior and DA neurotransmission appears largely mediated via nicotinic receptors (nAChRs) in the ventral tegmental area (VTA). The nAChR antagonist mecamylamine administered systemically in chronically nicotine-treated rats elicits a behavioral withdrawal syndrome concomitant with a reduced DA output in the nucleus accumbens (NAC). Here, we investigated the behavioral and biochemical consequences of intrategmental administration of mecamylamine in rats chronically infused with nicotine by means of minipumps for 14 days (9 mg/kg/day). Bilateral, intrategmental mecamylamine injections (1, 3 or 9 g/0.5 l/ side) dose-dependently increased abstinence signs such as gasps, teeth chatter, and reduced locomotor activity in nicotine-treated, but not in control animals. Moreover, a unilateral intrategmental injection of 9 g mecamylamine reduced DA output in the ipsilateralThe habit of tobacco smoking is widely considered to represent a form of drug addiction to nicotine (Clarke 1990;Corrigall et al. 1992) and, in fact, constitutes the leading preventable cause of human morbidity and premature mortality in the US (US Department of Health and Human Services 1988). Although smokers are usually aware of the negative health consequences of their habit, the prognosis of successful smoking cessation is relatively poor. Thus, approximately 80% of smokers enrolled in cessation programmes fail to quit (Stitzer and Gross 1988). A nicotine withdrawal reaction, which usually emerges within 24 hrs after the last cigarette, is considered to significantly contribute to the high relapse rate during the early stages of attempted cessation (Shiffman and Jarvik 1976;Hughes et al. 1992;Killen et al. 1991;West et al. 1989), although a lack of correlation Received December 10, 1998; revised April 7, 1999; accepted April 20, 1999. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO . 4 Role of VTA Nicotinic Receptors in Nicotine Withdrawal 561 between withdrawal severity and probability for relapse has been reported in other studies (see Hughes et al. 1991).In rats chronically treated with nicotine, sudden withdrawal precipitated by systemic administration of the non-competitive nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine (Malin et al. 1994;Hildebrand et al. 1997), as well as spontaneous withdrawal caused by termination of a chronic nicotine infusion (Malin et al. 1992;Hildebrand et al. 1997), produces behavioral symptoms similar to those described in opiate withdrawal (see Bläsig et al. 1973). Acute as well as chronic administration of nicotine increases locomotor activity in rats (Benwell and Balfour 1992;Clarke and Kumar 1983;Stolerman et al. 1973), whereas in nicotine withdrawal locomotor activity is markedly reduced (Malin et al. 1992(Malin et al. , 1994Hildebrand et al. 1997).Compelling evidence indicates that the mesolimbic dopamine (DA) system plays a pivotal role in mediati...

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Nicotine induced c-fos expression in the striatum is mediated mostly by dopamine D1 receptor and is dependent on NMDA stimulation

Cited by 81 publications

References 58 publications

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

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

Chronic Nicotine Enhances Basal and Nicotine-Induced Fos Immunoreactivity Preferentially in the Medial Prefrontal Cortex of the Rat

Behavioral and Biochemical Manifestations of Mecamylamine-Precipitated Nicotine Withdrawal in the Rat Role of Nicotinic Receptors in the Ventral Tegmental Area

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