Morphine induces c-fos and junB in striatum and nucleus accumbens via D1 and N-methyl-D-aspartate receptors.

Liu, Jialing; Nickolenko, Jeremy; Sharp, Frank R.

doi:10.1073/pnas.91.18.8537

Cited by 169 publications

(92 citation statements)

References 74 publications

(105 reference statements)

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“…The general pattern of immediate early gene (IEG) expression elicited by morphine in the present study (eg, c-fos induction primarily in the most dorsomedial portion of the CPu and cingulate cortex) is consistent with the existing literature (Liu et al, 1994;Garcia et al, 1995;Curran et al, 1996;Erdtmann-Vourliotis et al, 1999b;Frankel et al, 1999b; see Harlan and Garcia (1998) for review). Our results are also consistent with a recent report showing that morphine administration in a stressful environment induces greater c-fos expression in the dorsomedial CPu than morphine administration in a calm environment (Mayer et al, 2002).…”

Section: Morphine-induced C-fos Expression In the Striatopallidal Patsupporting

confidence: 90%

“…Studies examining the mechanisms underlying morphineevoked IEG expression in the CPu have established that coactivation of m opioid and dopamine receptors is required for IEG induction to occur (Liu et al, 1994;Sharp et al, 1995;Bontempi and Sharp, 1997;Frankel et al, 1999a). Morphine is thought to act at m opioid receptors to disinhibit mesolimbic dopamine neurons, resulting in increased dopamine release in the CPu (Matthews and German, 1984;Di Chiara and North, 1992;Johnson and North, 1992;Spanagel et al, 1992;Devine et al, 1993).…”

Section: Morphine-induced C-fos Expression In the Striatopallidal Patmentioning

confidence: 99%

“…Dopamine is then thought to induce IEG expression via D1 receptor activation of the cAMP/PKA signaling cascade (Lovenberg et al, 1991;Cole et al, 1994;Konradi et al, 1994Konradi et al, , 1996. In addition, the ability of morphine to induce IEGs is strongly regulated by glutamate, as NMDA receptor antagonists (Liu et al, 1994;Bontempi and Sharp, 1997;D'Souza et al, 1999), AMPA receptor antagonists (Garcia et al, 2003), and metabotropic glutamate receptor antagonists (Garcia et al, 2003) all attenuate morphine-evoked IEG expression in the CPu.…”

Section: Morphine-induced C-fos Expression In the Striatopallidal Patmentioning

confidence: 99%

“…The present study shows that morphine administration in a novel test environment also induces this pattern of striatonigral cellular activation. Although the mechanism of this activation in either case is not yet clear, the fact that antagonists of either dopamine or glutamate receptors block both morphine-and psychostimulant-evoked c-fos expression in EnkÀ cells (Liu et al, 1994;Ferguson et al, 2003) suggests that this regulation may be occurring through a common mechanism.…”

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

confidence: 99%

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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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Section: Morphine-induced C-fos Expression In the Striatopallidal Patsupporting

confidence: 90%

Section: Morphine-induced C-fos Expression In the Striatopallidal Patmentioning

confidence: 99%

Section: Morphine-induced C-fos Expression In the Striatopallidal Patmentioning

confidence: 99%

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

confidence: 99%

See 2 more Smart Citations

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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“…Recently, we have demonstrated a D 1 -receptor mediated increase in Fos-like immunoreactivity (FLI) in several limbic regions of the brain after burst-like electrical stimulation of the median forebrain bundle . 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).…”

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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Effects of phencyclidine on immediate early gene expression in the brain

et al. 1996

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The N‐methyl‐D‐aspartate receptor antagonist phencyclidine (PCP) is a psychotomimetic drug which produces schizophrenia‐like psychosis. In animal studies it is toxic to neurons in the posterior cingulate and retrosplenial cortex and to cerebellar Purkinje cells. To find clues about the mechanism and pathways of PCP action, we studied the effect of systemic PCP administration (10 and 50 mg/kg, intraperitoneal) on the expression of immediate‐early genes (IEGs) (c‐fos, c‐jun, egr‐2, egr‐3, NGFI‐A, NGFI‐B, NGFI‐C, and Nurr1) using in situ hybridization histochemistry. PCP, 50 mg/kg, produced a biphasic IEG induction: an early induction in the hippocampus, cerebral cortex, and cerebellar granule cell layer, and a delayed induction in the posterior cingulate cortex and cerebellar Purkinje cell layer. The early induction of all eight IEGs was observed 30 min after drug treatment in the cerebral cortex and in the hippocampus. c‐fos, NGFI‐A, and NGFI‐B were also induced in thalamic nuclei, and c‐fos was also induced in the cerebellar granule cell layer. In contrast, a delayed induction of c‐fos, c‐jun, NGFI‐A, NGFI‐B, NGFI‐C, and Nurr1 in the posterior cingulate cortex was observed 2–6 hr after PCP, 50 mg/kg. egr‐2 and egr‐3 were not induced in the posterior cingulate cortex. c‐fos induction in the cerebellar Purkinje cell layer peaked 2 hr after PCP, 50 mg/kg. In addition, PCP induced c‐fos, egr‐3, NGFI‐A NGFI‐B, NGFI‐C, and Nurr1 in the inferior olivary nucleus. PCP‐induced IEG expression returned to baseline by 24 hr. A lower PCP dose, 10 mg/kg, induced lower levels of IEG expression, with similar anatomical and biphasic temporal pattern as with the higher PCP dose of 50 mg/kg. However, no IEG induction was observed in the hippocampus following 10 mg/kg PCP. These results demonstrate that PCP produces neural activation not only in the cingulate and retrosplenial cortex, but also in many other regions of forebrain and cerebellum. Moreover, prolonged IEG expression in the posterior cingulate cortex and cerebellar Purkinje cells, the sites of PCP toxicity, suggests that IEGs could mediate neurotoxic/neuroprotective effects in these brain regions. © 1996 Wiley‐Liss, Inc.

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Morphine induces c-fos and junB in striatum and nucleus accumbens via D1 and N-methyl-D-aspartate receptors.

Cited by 169 publications

References 74 publications

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

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

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

Effects of phencyclidine on immediate early gene expression in the brain

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