Coordinate expression of c-fos and jun B is induced in the rat striatum by cocaine

Moratalla, Rosario; Ea, Vickers; Ha, Robertson; Cochran, Brent; Graybiel, Ann M.

doi:10.1523/jneurosci.13-02-00423.1993

Cited by 151 publications

(98 citation statements)

References 72 publications

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“…Male mice were given injections of saline (n ϭ 6 for each genotype) or 25 mg/kg cocaine (cKO, n ϭ 4; Ctrl, n ϭ 5) 30 min before being killed by cervical dislocation. This time interval was chosen because mRNA levels of both Nur77 and c-fos are high at this point (Moratalla et al, 1993;Dragunow et al, 1996). Brains were rapidly removed and frozen in isopentane at Ϫ40°C.…”

Section: Methodsmentioning

confidence: 99%

Enhanced Sucrose and Cocaine Self-Administration and Cue-Induced Drug Seeking after Loss of VGLUT2 in Midbrain Dopamine Neurons in Mice

Alsiö¹,

Nordenankar²,

Arvidsson³

et al. 2011

J. Neurosci.

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Themesostriataldopamine(DA)systemcontributestoseveralaspectsofresponsestorewardingsubstancesandisimplicatedinconditionssuch asdrugaddictionandeatingdisorders.AsubsetofDAneuronshasbeenshowntoexpressthetype2Vesicularglutamatetransporter(Vglut2)and may therefore corelease glutamate. In the present study, we analyzed mice with a conditional deletion of Vglut2 in DA neurons (Vglut2 f/f;DAT-Cre ) to address the functional significance of the glutamate-DA cophenotype for responses to cocaine and food reinforcement. Biochemical parameters of striatal DA function were also examined by using DA receptor autoradiography, immediate-early gene quantitative in situ hybridization after cocaine challenge, and DA-selective in vivo chronoamperometry. Mice in which Vglut2 expression had been abrogated in DA neurons displayed enhanced operant self-administration of both high-sucrose food and intravenous cocaine. Furthermore, cocaine seeking maintained by drug-paired cues was increased by 76%, showing that reward-dependent plasticity is perturbed in these mice. In addition, several lines of evidence suggest that adaptive changes occurred in both the ventral and dorsal striatum in the absence of VGLUT2: DA receptor binding was increased, and basal mRNA levels of the DA-induced early genes Nur77 and c-fos were elevated as after cocaine induction. Furthermore, in vivo challenge of the DA system by potassium-evoked depolarization revealed less DA release in both striatal areas. This study demonstrates that absence of VGLUT2 in DA neurons leads to perturbations of reward consumption as well as reward-associated memory, features of particular relevance for addictive-like behavior.

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Section: Methodsmentioning

confidence: 99%

Enhanced Sucrose and Cocaine Self-Administration and Cue-Induced Drug Seeking after Loss of VGLUT2 in Midbrain Dopamine Neurons in Mice

Alsiö¹,

Nordenankar²,

Arvidsson³

et al. 2011

J. Neurosci.

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“…KGoine, Sweden. and have been t&ted for specificity (W&den et al, 1996;Moratalla et al, 1993;Johansson et al, 1994). Oligodeoxynucleotide probes were radiolabeled using terminal deoxynucleotidyl transferase (Pharmacia LKB, Uppsala, Sweden) and &?S-dATP (Du Pant, New England Nuclear, Stockholm, Sweden) to a specific activity of about to" cpm/pg.…”

Section: Methodsmentioning

confidence: 99%

Biphasic changes in locomotor behavior and in expression of mRNA for NGFI-A and NGFI-B in rat striatum following acute caffeine administration

1995

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The time course of expression of mRNA for NGFI-A and NGFI-B after a single intraperitoneal injection of saline or caffeine was examined using in situ hybridization. Administration of a high dose of caffeine (100 mg/kg) decreased locomotor behavior and increased NGFI-A and NGFI- B mRNA in the entire striatum. A lower dose of caffeine (50 mg/kg) caused a weak enhancement of both messages, which was confined to the lateral part of caudate-putamen. This dose increased horizontal, but not vertical, movement. In rats treated with the lowest dose of caffeine (25 mg/kg), the expression of both investigated genes tended to be lower than for saline-treated rats and both horizontal and vertical locomotor activity increased markedly. The reduction in the number of labeled neurons seemed to occur predominantly in enkephalin- containing neurons, which coexpress adenosine A2A receptors and dopamine D2 receptors. The decrease of mRNA for NGFI-A, NGFI-B, and jun B caused by caffeine (25 mg/kg) could be mimicked by the D2 agonist quinpirole (1 and 3 mg/kg). Moreover, caffeine could significantly decrease the expression seen following treatment with the D2 antagonist raclopride (2 mg/kg). In addition, in the parietal cortex, 25 mg/kg of caffeine caused a significant elevation of both examined immediate early genes. Thus, biphasic changes in locomotion induced by caffeine are paralleled by biphasic changes in mRNA for NGFI-A, NGFI-B, and jun B. The results also provide additional support for a functionally important interaction between adenosine and dopamine D2 receptors.

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“…Cocaine increases DA release in the striatum through the blockade of transporter-mediated DA reuptake from nigrostriatal nerve endings and causes rapid induction of striatal c-fos, a commonly used molecular marker for neuronal activity. This effect is fully sensitive to DA receptor blockade (Graybiel et al, 1990;Moratalla et al, 1993), indicating that the actions of cocaine in the striatum are mediated, largely if not exclusively, by the release of endogenous DA and consequent DA receptor stimulation. Other mechanisms, however, might be involved in the pharmacological actions of cocaine in the striatum.…”

Section: Involvement Of the Striatum In Cocaine Addictionmentioning

confidence: 96%

A Critical Interaction between Dopamine D2 Receptors and Endocannabinoids Mediates the Effects of Cocaine on Striatal GABAergic Transmission

Centonze

Battista

Rossi

et al. 2004

Neuropsychopharmacol

136

112

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Compelling evidence indicates that endocannabinoids are implicated in drug addiction. In the present study, we have addressed the interaction between cocaine and endocannabinoid system by means of neurochemical and neurophysiological experiments in rat brain slices. Using gas chromatography-electron impact mass spectrometry, we have found that cocaine increased the levels of the endocannabinoid anandamide in the striatum, a brain area primarily involved in the compulsive drug-seeking and drug-taking behaviors typical of addiction. This effect was attenuated by pharmacological inhibition of D2-like receptors but not D1-like receptors, and it was mimicked by D2-like but not D1-like receptor stimulation. The cocaine-induced increase in anandamide concentrations was attributable to both stimulation of its synthesis and inhibition of its degradation, as suggested by the ability of cocaine and quinpirole, a D2-like receptor agonist, to enhance the activity of NAPE-phospholipase D and to inhibit fatty acid amide hydrolase. By means of electrophysiological recordings from single striatal neurons, we have then observed that the ability of cocaine to inhibit, via D2-like receptors, GABA transmission was partially prevented following blockade of cannabinoid receptors, suggesting that endocannabinoids may act as downstream effectors in the action of cocaine in the striatum. Understanding the molecular and physiological effects of drugs of abuse in the brain is essential for the development of effective strategies against addiction.

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Coordinate expression of c-fos and jun B is induced in the rat striatum by cocaine

Cited by 151 publications

References 72 publications

Enhanced Sucrose and Cocaine Self-Administration and Cue-Induced Drug Seeking after Loss of VGLUT2 in Midbrain Dopamine Neurons in Mice

Enhanced Sucrose and Cocaine Self-Administration and Cue-Induced Drug Seeking after Loss of VGLUT2 in Midbrain Dopamine Neurons in Mice

Biphasic changes in locomotor behavior and in expression of mRNA for NGFI-A and NGFI-B in rat striatum following acute caffeine administration

A Critical Interaction between Dopamine D2 Receptors and Endocannabinoids Mediates the Effects of Cocaine on Striatal GABAergic Transmission

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