Cocaine and amphetamine preferentially stimulate glutamate release in the limbic system: Studies on the involvement of dopamine

Reid, Malcolm S.; Hsu, Kang; Berger, Stanley A.

doi:10.1002/(sici)1098-2396(199710)27:2<95::aid-syn1>3.0.co;2-6

Cited by 188 publications

(123 citation statements)

References 58 publications

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“…While methamphetamine's effects upon the monoaminergic systems have received considerable experimental attention [for reviews, [264][265][266][267][268][269][270], less is known regarding the regulation of corticoaccumbens glutamate and glutamate receptor expression by amphetamine and methylated analogs. Acute administration of amphetamines is reported to produce either no change or a delayed rise in extracellular glutamate levels within striatal regions [59][60][61][62]271,272], while an acute injection of methamphetamine, but not amphetamine, elevates PFC glutamate levels [271]. Whereas repeated cocaine administration produces robust drug-induced glutamate sensitization within the NAC [e.g., 31,35,47,57], repeated dosing with non-toxic regimens of amphetamine or methamphetamine elicits little effect upon the capacity of these drugs to alter glutamate levels within the corticoaccumbens pathway [61,272].…”

Section: Homers and Methamphetaminementioning

confidence: 99%

Homers regulate drug-induced neuroplasticity: Implications for addiction

Szumlinski

Ary

Lominac

2008

Biochemical Pharmacology

118

160

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Drug addiction is a chronic, relapsing disorder, characterized by an uncontrollable motivation to seek and use drugs. Converging clinical and preclinical observations implicate pathologies within the corticolimbic glutamate system in the genetic predisposition to, and the development of, an addicted phenotype. Such observations pose cellular factors regulating glutamate transmission as likely molecular candidates in the etiology of addiction. Members of the Homer family of proteins regulate signal transduction through, and the trafficking of, glutamate receptors, as well as maintain and regulate extracellular glutamate levels in corticolimbic brain regions. This review summarizes the existing data implicating the Homer family of protein in acute behavioral and neurochemical sensitivity to drugs of abuse, the development of drug-induced neuroplasticity, as well as other behavioral and cognitive pathologies associated with an addicted state.

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Section: Homers and Methamphetaminementioning

confidence: 99%

Homers regulate drug-induced neuroplasticity: Implications for addiction

Szumlinski

Ary

Lominac

2008

Biochemical Pharmacology

118

160

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“…Acute administration of morphine, which decreases the number of novelty-evoked c-fos/Enk þ cells, concomitantly decreases the number of novelty-evoked cfos þ cells in cingulate cortex, as well as firing of cortical neurons Henriksen, 1996, 1998) and corticostriatal glutamate release (Desole et al, 1996;Nicol et al, 1996). By contrast, at doses that activate Enk þ cells, psychostimulants increase novelty-evoked c-fos expression in cingulate cortex (Badiani et al, 1998) and stimulate corticostriatal glutamate release (Smith et al, 1995;Reid et al, 1997;Gray et al, 1999). Furthermore, transection of corticostriatal afferents leads to a selective blockade of psychostimulant-evoked c-fos expression in Enk þ cells (SMF and TER unpublished observations).…”

Section: Morphine Induces a Different Pattern Of Gene Expression In Tmentioning

confidence: 99%

Morphine-Induced c-fos mRNA Expression in Striatofugal Circuits: Modulation by Dose, Environmental Context, and Drug History

Ferguson

Thomas

Robinson

2004

Neuropsychopharmacol

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Opiates and psychostimulants produce many shared behavioral and neurobiological adaptations, such as behavioral sensitization and the induction of immediate early genes in the caudate-putamen (CPu). Previous studies indicate that factors such as dose, the environmental context surrounding drug administration and drug history can influence both morphine-and psychostimulant-induced behavioral sensitization. In addition, these factors can modulate the ability of psychostimulants to engage striatofugal circuits in the CPu. The present study, therefore, sought to examine whether these factors have similar influences over the ability of morphine to engage corticostriatofugal circuits. We report that, when given in the home cage, morphine produced a small, but significant increase in the number of c-fos þ striatonigral cells and c-fos þ cells in cingulate cortex, but had no effect on the number of c-fos þ striatopallidal cells. When given in a novel test environment, however, morphine dramatically increased the number of c-fos þ striatonigral cells in a dose-dependent fashion, and this effect was maintained following repeated treatment. Unexpectedly, morphine treatment in a novel environment produced a dose-dependent reduction in the number of c-fos þ striatopallidal cells and c-fos þ cells in cingulate cortex, relative to exposure to novelty aloneFeffects that were reversed by repeated morphine treatment. We suggest that alterations in c-fos expression patterns in striatofugal circuits following morphine administration may be involved in drug-experience-dependent plasticity.

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“…The acute systemic administration of a high dose of cocaine increases extracellular glutamate in the nucleus accumbens (Smith et al 1995;Reid et al 1997), and after repeated cocaine treatment a lower dose of cocaine produces a rapid and enduring elevation in extracellular Figure 3. The time course of the behavioral data showing the capacity of CNQX to inhibit cocaine induced motor activity in the group of rats that were pretreated with daily cocaine in the test environment.…”

Section: Glutamate Transmission and Cocainementioning

confidence: 99%

Context-specific Enhancement of Glutamate Transmission by Cocaine

Bell

Duffy

Kalivas

2000

Neuropsychopharmacology

131

120

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The repeated injection of cocaine causes an increase in the capacity of a subsequent acute injection to elevate extracellular glutamate levels in the nucleus accumbens, and the present study sought to determine if the elevation in extracellular glutamate is regulated by the pairing of environmental stimuli with drug administration. Three treatment groups were injected daily for seven days with saline or cocaine (15 mg/kg, ip); 1) injection of saline in the home cage, 2) injection of cocaine in the home cage (cocaineunpaired), and 3) injection of cocaine in the test apparatus (cocaine-paired). Three weeks following the last daily injection dialysis probes were placed into the nucleus accumbens and all rats were injected with saline followed by cocaine. Basal levels of extracellular glutamate were significantly reduced in the cocaine-paired treatment group. The repeated administration of amphetamine-like psychostimulants produces enduring alterations in the behavioral response to subsequent drug administration. The behavioral adaptations include the induction of paranoia in humans, which has been modeled in rodents as the induction of a sensitized motor stimulant response to psychostimulant injection (Kokkinidis and Anisman 1980;Segal and Schuckit 1983;Robinson and Becker 1986). This animal model has been extensively employed over the last decade to elucidate the cellular adaptations that underlie the behavioral changes associated with repeated psychostimulant use. The research effort has been guided by two facts; 1) a critical molecular site of action for amphetamine-like psychostimulants is the dopamine transporter (Reith et al. 1986;Ritz et al. 1990; although see Rocha et al. 1998), and 2) dopa- NO . 3 mine transmission in the mesocorticolimbic dopamine projection from the ventral tegmental area to the nucleus accumbens is critical for the rewarding and motor stimulant actions of this class of drugs (Koob et al. 1993). Knowledge of the molecular action has precipitated the discovery of many cocaine-induced, dopamine-dependent neuroadaptations in the nucleus accumbens (see Nestler et al. 1993; White and Kalivas 1998, for reviews). Arising from this considerable research effort is the awareness that neither the emphasis on dopamine transmission nor the focus on the nucleus accumbens provides a complete profile of the neuroadaptations produced by repeated cocaine (Pierce and Kalivas 1997;Bardo 1998;Wolf 1998). Moreover, only in the cocaine-paired group did the cocaine injection elevate extracellular glutamate. Repeated administration of cocaine also produces an enduring increase in the motor stimulant response to an acute cocaine injection and it was previously found that administration of the ␣ -amino-3-hydroxy-5-methylisoxazole-4-propionic acid and kainic acid glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione inhibited the sensitized, but not the acute motor, response to cocaine. In this study it was found that the motor stimulant response elicited by cocaine was blunted by pretreatment of t...

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Cocaine and amphetamine preferentially stimulate glutamate release in the limbic system: Studies on the involvement of dopamine

Cited by 188 publications

References 58 publications

Homers regulate drug-induced neuroplasticity: Implications for addiction

Homers regulate drug-induced neuroplasticity: Implications for addiction

Morphine-Induced c-fos mRNA Expression in Striatofugal Circuits: Modulation by Dose, Environmental Context, and Drug History

Context-specific Enhancement of Glutamate Transmission by Cocaine

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