Clonidine Reduces Dopamine and Increases GABA in the Nucleus Accumbens

Murai, Tameatsu; Yoshida, Yukihiro; Koide, Shigeyo; Takada, Koji; Misaki, Toru; Koshikawa, Noriaki; Cools, Alexander R.

doi:10.1016/s0091-3057(98)00050-1

Cited by 28 publications

(10 citation statements)

References 27 publications

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“…Previous studies have reported a 2 -AR mediated regulation of accumbal DA release with both local and systemic administration of a 2 -AR selective drugs. However, the evidence of local regulatory mechanism comes from studies using slice preparations (Russell et al 1993;de Villiers et al 1995), whereas all in vivo studies so far have employed systemic administration of a 2 -AR active drugs (Yavich et al 1997;Murai et al 1998;Whittington et al 2001). Also in contrast to the present study, local application of a 2 -AR active drugs did not affect NA release in the NAc slice (Schoffelmeer et al 1998).…”

Section: Discussioncontrasting

confidence: 65%

“…1995), whereas all in vivo studies so far have employed systemic administration of α 2 ‐AR active drugs (Yavich et al . 1997; Murai et al . 1998; Whittington et al .…”

Section: Discussionmentioning

confidence: 99%

“…The NAc receives a dense dopaminergic innervation from the mesolimbic nuclei of ventral tegmental area (VTA) and adrenergic innervation from the locus coeruleus and other brainstem adrenergic nuclei (Phillipson 1979). Evidence from several studies indicates that noradrenaline (NA) projections can regulate dopaminergic activity in the NAc and that this regulation involves a 2 -adrenoceptors (a 2 -ARs) (Russell et al 1993;de Villiers et al 1995;Yavich et al 1997;Murai et al 1998;Whittington et al 2001). However, it is not known which a 2 -AR subtypes are involved in this regulation and whether a 2 -AR-mediated control of DA and NA release originates from the brainstem nuclei or at the terminal level in the NAc.…”

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confidence: 99%

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In vivo regulation of dopamine and noradrenaline release by alpha2A‐adrenoceptors in the mouse nucleus accumbens

Ihalainen

Tanila

2004

Journal of Neurochemistry

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The present study investigated the role of alpha2A-adrenoceptor (a 2A -AR) subtype in the regulation of noradrenaline (NA) and dopamine (DA) release in the nucleus accumbens (NAc). The effect of locally infused and systemically injected a 2 -AR agonist, dexmedetomidine (DMT), and a 2 -AR antagonist, atipamezole, on NA and DA release was investigated in a 2A -AR knockout and control mice by using in vivo microdialysis. In addition, we compared the drug effects on DA and NA release in the NAc to their effect on locomotor activity. Baseline NA and DA concentrations did not differ between genotypes. Local infusion of DMT decreased, in a concentration-dependent manner, NA, but not DA, levels in the control mice. However, systemic injection of DMT decreased both NA and DA levels in the control mice. In both cases DMT had no effects on transmitter release in a 2A -AR knockout mice. Our results suggest that a 2 -ARs regulate the release of NA, but not DA, at the terminal level in the NAc. However, a 2 -ARs regulate DA release in the NAc indirectly by their effect on DA neurones in the ventral tegmental area via an unknown mechanism. In both cases the regulation is mediated by a 2A -adrenoceptor subtype. Also the modulation of locomotor activity by a 2 -AR agonist and antagonist seems to be mediated via a 2A -adrenoceptors.

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Section: Discussioncontrasting

confidence: 65%

“…1995), whereas all in vivo studies so far have employed systemic administration of α 2 ‐AR active drugs (Yavich et al . 1997; Murai et al . 1998; Whittington et al .…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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In vivo regulation of dopamine and noradrenaline release by alpha2A‐adrenoceptors in the mouse nucleus accumbens

Ihalainen

Tanila

2004

Journal of Neurochemistry

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“…It is interesting, however, that clonidine is known to have effects on the functioning of midbrain dopaminergic neurons (Lategan et al 1990). For example, it has been shown that systemic injections of alpha-2 adrenergic receptor agonists decrease dopamine release in the nucleus accumbens (Murai et al 1998) and the PFC (Gobert et al 1998). These effects may be due to the effect of alpha-2 adrenergic receptor agonists on dopamine cell firing.…”

Section: Discussionmentioning

confidence: 99%

Alpha-2 Adrenergic Receptor Agonists Block Stress-Induced Reinstatement of Cocaine Seeking

Erb

Hitchcott

Rajabi

et al. 2000

Neuropsychopharmacology

241

193

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The alpha -2 adrenergic receptor agonists, clonidine, lofexidine and guanabenz, blocked stress-but not cocaineinduced reinstatement of cocaine seeking at doses that suppressed footshock-induced release of noradrenaline in prefrontal cortex and amygdala. Rats were trained to selfadminister cocaine (0.5 mg/kg/infusion, i.v; 10-12 days) and, after a drug-free period (7-13 days), were returned to the selfadministration chambers for daily extinction and reinstatement test sessions. Both intermittent footshock (15 min, 0.6 mA) and cocaine priming (20 mg/kg, i.p.) reinstated extinguished drug seeking. Pretreatment with eitherclonidine (20, or 40 g/kg, i.p.) or lofexidine (50, 100, 150, or 200 g/kg, i.p.) (e.g. Jaffe 1985) and reinstate drug-seeking in monkeys and rats with a history of drug self-administration (e.g., Stretch and Gerber 1973;de Wit and Stewart 1981). Another factor thought to be important to relapse in humans is stress (Kreek and Koob 1998). In a recent laboratory study, Sinha and colleagues (1999) found that induction of psychological stress provoked craving for drug in cocaine addicts. Using an animal model of stress-induced relapse, we and others have found in rats that exposure to brief intermittent footshock stress reliably reinstates heroin seeking (Shaham and Stewart 1995), cocaine seeking (Erb et al. 1996;Ahmed and Koob 1997;Mantsch and Goeders 1999), nicotine seeking (Buczek et al. 1999), and alcohol seeking (Lê et al. 1998).In a search for neurotransmitter systems involved in stress-induced relapse, and for pharmacological manipulations that might prevent it, we explored in the present set of experiments the role of the noradrenergic (NE) system, comprised of a dorsal stream of neurons originating in the locus-coeruleus and a ventral stream of neurons originating in the lateral tegmental nuclei (Aston-Jones et al. 1995;Moore and Bloom 1979). Although the stress-related functions of the ventral projections have been only partially characterized (Cole and Robbins 1987;Hansen et al. 1980), NE projections from the LC have been directly implicated in a number From the Center for Studies in Behavioral Neurobiology (SE, PKH, HR, DM, JS), Department of Psychology, Concordia University, Montreal, Quebec, Canada; Behavioral Neuroscience Department(YS), IRP/NIDA, Baltimore, MD.Address correspondence to: Dr. Jane Stewart, Center for Studies in Behavioral Neurobiology, Department of Psychology, 1455 de Maisonneuve Blvd. W., Montreal, Quebec, Canada H3G 1M8 Tel: 514-848-2193, Fax: 514-848-2817, E-mail: Stewart@CSBN.concordia.ca. Received September 20, 1999 revised December 21, 1999; accepted December 28, 1999. N EUROPSYCHOPHARMACOLOGY 2000 -VOL . 23 , NO . 2 alpha -2 Agonists and Relapse to Cocaine Seeking 139 of stress-related responses. For example, electrical stimulation of the LC has been found to induce anxiety and to result in activation of the autonomic nervous system, whereas local injections of the alpha-2 adrenergic receptor agonist clonidine, which acts to inhibit NE cell fi...

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“…Diazepam has been widely used as an anxiolytic medication and clonidine has also been found to decrease anxiety (Hoehn-Saric et al 1981). Like clonidine, diazepam can decrease firing of the locus coeruleus (Grant et al 1980), attenuate both basal and stress induced NE release in the mPFC (Rossetti et al 1990), attenuate dopamine release in the nucleus accumbens (Murai et al 1998), and attenuate sensory evoked acetylcholine release in the medial PFC in rodents (Acquas et al 1998). In order to address the possibility that clonidine may be effecting task performance indirectly by altering measures also effected by diazepam, the current study also characterized delayed response performance in young monkeys following diazepam treatment (1.0, 2.0, and 3.0 mg/kg).…”

mentioning

confidence: 99%

Treatment with the Noradrenergic Alpha-2 Agonist Clonidine, But Not Diazepam, Improves Spatial Working Memory in Normal Young Rhesus Monkeys

Franowicz

Arnsten

1999

Neuropsychopharmacology

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Clonidine Reduces Dopamine and Increases GABA in the Nucleus Accumbens

Cited by 28 publications

References 27 publications

In vivo regulation of dopamine and noradrenaline release by alpha2A‐adrenoceptors in the mouse nucleus accumbens

In vivo regulation of dopamine and noradrenaline release by alpha2A‐adrenoceptors in the mouse nucleus accumbens

Alpha-2 Adrenergic Receptor Agonists Block Stress-Induced Reinstatement of Cocaine Seeking

Treatment with the Noradrenergic Alpha-2 Agonist Clonidine, But Not Diazepam, Improves Spatial Working Memory in Normal Young Rhesus Monkeys

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