NMDA and D1 receptors mediate induction of c-fos and junB genes in striatum following morphine administration: implications for studies of memory

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

doi:10.1016/0166-4328(94)00146-7

Cited by 38 publications

(18 citation statements)

References 45 publications

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“…Such an influence therefore would not be apparent under basal conditions but would play a role in determining the net effect of systemic D-amphetamine on striatal ACh efflux. A permissive relation between glutamate transmission and D 1 activity in regulating neuronal f unction in the striatum has been observed previously for a number of variables including striatal GABA release, NMDA-mediated excitation of striatal cells, and Fos induction in striatal neurons (C epeda et al, 1993;Morari et al, 1994;Sharp et al, 1995;Wang and Johnson, 1995). Finally, in the striatum a 2 mg/kg dose of D-amphetamine has been shown to increase dialysate concentrations of dopamine from 28 to ϳ700 nM and also to increase dialysate concentrations of 5-HT from 1 to ϳ7 nM (Kuczenski et al, 1995).…”

Section: Discussionsupporting

confidence: 62%

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Abercrombie

Deboer

1997

J. Neurosci.

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Dopamine release can regulate striatal acetylcholine efflux in vivo through at least two receptor mechanisms: (1) direct inhibition by dopamine D 2 receptors on the cholinergic neurons, and (2) excitation initiated by dopamine D 1 receptors. The neuroanatomical locus of the latter population of D 1 receptors and the pathway(s) involved in the expression of their influence are controversial issues. We have tested the hypothesis that D 1 receptors in substantia nigra pars reticulata are involved in the excitatory component of dopaminergic actions on striatal acetylcholine output. In vivo microdialysis was used in awake rats. Infusion of the selective D 1 receptor agonist R(ϩ)-1-Phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol (SKF 38393) hydrochloride into pars reticulata of substantia nigra elicited a significant increase in striatal acetylcholine efflux. Likewise, D-amphetamine applied into pars reticulata of substantia nigra by reverse dialysis produced an elevation in acetylcholine output measured at a second microdialysis probe in the striatum. Application of D-amphetamine in the striatum by reverse dialysis elicited a decrease in striatal acetylcholine efflux that could be reversed subsequently by local application of Damphetamine in substantia nigra pars reticulata. A 2 mg/kg intraperitoneal dose of D-amphetamine, which has no net effect on striatal acetylcholine output under control conditions, elicited a significant decrease in acetylcholine efflux when the D 1 receptor antagonist R(ϩ)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SCH 23390) hydrochloride was applied simultaneously via a second microdialysis probe in substantia nigra pars reticulata. Thus, an excitatory D 1 -mediated influence on striatal acetylcholine output is initiated in substantia nigra pars reticulata, and this influence contributes to the effects of indirect dopaminergic agonists such as D-amphetamine on striatal acetylcholine efflux. These results indicate an important role of somatodendritic dopamine release, in addition to nerve terminal dopamine release, in the regulation of activity in basal ganglia circuits.

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Section: Discussionsupporting

confidence: 62%

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Abercrombie

Deboer

1997

J. Neurosci.

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“…[8,20,33,35]) and glutamatergic (e.g. [17,27,30]) systems may also mediate opiate-induced reward or locomotor activity. Strain differences in basal anxiety level may also be important determinants in the expression of conditioned place preference.…”

Section: Discussionmentioning

confidence: 99%

Heroin-induced locomotor activity and conditioned place preference in C57BL/6J and 129P3/J mice

Schlussman

Zhang

Hsu

et al. 2008

Neuroscience Letters

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Differences in the locomotor stimulating and rewarding properties of drugs of abuse have been described in several inbred strains of mice, and comparisons of inbred strains with differing responses to drugs of abuse may provide crucial insight into the question of individual vulnerability to the effects of drugs of abuse. The present study was designed to examine the rewarding and locomotorstimulating effects of heroin in C57BL/6J and 129P3/J mice. Heroin produced a robust dose dependent locomotor stimulation in both strains. Both strains also developed conditioned place preference to heroin, again in a dose dependent manner. However C57BL/6J mice developed conditioned place preference to only the two lowest doses of heroin tested, while the 129P3/J counterparts showed conditioned place preference to only the three highest doses tested. These studies indicate that 129P3/J mice are less sensitive to the rewarding effects of heroin than are agematched C57BL/6J mice.

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“…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%

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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NMDA and D1 receptors mediate induction of c-fos and junB genes in striatum following morphine administration: implications for studies of memory

Cited by 38 publications

References 45 publications

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Heroin-induced locomotor activity and conditioned place preference in C57BL/6J and 129P3/J mice

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

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NMDA and D1 receptors mediate induction of c-fos and junB genes in striatum following morphine administration: implications for studies of memory

Cited by 38 publications

References 45 publications

Substantia Nigra D1Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Substantia Nigra D1Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Heroin-induced locomotor activity and conditioned place preference in C57BL/6J and 129P3/J mice

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

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Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism

Substantia Nigra D₁Receptors and Stimulation of Striatal Cholinergic Interneurons by Dopamine: A Proposed Circuit Mechanism