Cortical stimulation induces Fos expression in striatal neurons via NMDA glutamate and dopamine receptors

Liste, Isabel; Rozas, G.; Guerra, María J.; Labandeira‐Garcia, Jose L.

doi:10.1016/0006-8993(95)00958-s

Cited by 54 publications

(39 citation statements)

References 69 publications

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“…Dopaminergic input to the DLS provides a signal that effectively imprints S-R associations (White, 1989). Glutamate and dopamine are involved in synaptogenesis (Petrak et al, 2005;Spencer et al, 1998) and activation of these two systems increase Fos expression in the DLS (Graybiel et al, 1990;Liste et al, 1995). The current findings indicate that the associative learning processes subsumed during AMPH-induced CMS may engage these, or similar systems, to alter synaptically mediated function in the DLS.…”

Section: Discussionmentioning

confidence: 70%

Context modulates the expression of conditioned motor sensitization, cellular activation and synaptophysin immunoreactivity

Rademacher

Napier

Meredith

2007

Eur J of Neuroscience

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We tested the hypothesis that amphetamine-(AMPH) induced conditioned motor sensitization is accompanied by cellular activation (measured by Fos immunoreactivity) and synaptophysin immunoreactivity in reward-related brain areas. Forty-eight rats were tested for conditioned motor sensitization using a conditioning paradigm that was performed in a three-chambered apparatus. Rats underwent two drug pairings with 1.0 mg/kg AMPH in one outer chamber and, on alternate days, were paired with saline in the other. On the fifth day, relative to the first AMPH treatment, AMPH administration increased motor activity in the AMPH-paired context but not in the saline-paired context. Relative to the first saline treatment, saline on the fifth day produced a conditioned increase in motor activity when given in the chamber previously paired with AMPH, and saline given in the saline-paired context produced a conditioned decrease in motor activity. AMPH administered in the AMPH-paired context increased the density of both Fos and synaptophysin immunoreactivity in the dentate gyrus, cornu ammonis (CA)1, CA3, basolateral amygdala, and dorsolateral striatum. This pairing between context and drug increased Fos but not synaptophysin immunoreactivity in the nucleus accumbens core and shell. Saline administered in the AMPH-paired context increased the density of Fos immunoreactivity in the basolateral amygdala and nucleus accumbens core. These data indicate that the basolateral amygdala-nucleus accumbens core pathway is necessary for the context-elicited conditioned motor responses, while the hippocampus encodes the spatial context.

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Section: Discussionmentioning

confidence: 70%

Context modulates the expression of conditioned motor sensitization, cellular activation and synaptophysin immunoreactivity

Rademacher

Napier

Meredith

2007

Eur J of Neuroscience

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“…In this context, cortical and nigral afferents to the striatum and interactions between the two afferent systems are particularly interesting. The striatal release of dopamine (DA) might be under glutamatergic control Baunez et al 1994;Martinez-Fong et al 1992;Whitton et al 1994), conversely, the release of glutamate and its postsynaptic effects might be under dopaminergic control (Carlsson and Carlsson 1990;Lindefors and Ungerstedt 1990;Liste et al 1995). These interactions are still poorly understood, and apparently conflicting data have been obtained under different experimental conditions.…”

Section: Introductionmentioning

confidence: 98%

Treadmill running induces striatal Fos expression via NMDA glutamate and dopamine receptors

et al. 1997

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Several non-physiological stimuli (i.e. pharmacological or electrical stimuli) have been shown to induce Fos expression in striatal neurons. In this work, striatal Fos (i.e. Fos-like) expression was studied after physiological stimulation, i.e. motor activity (treadmill running at 36 m/min for 20 min). In rats killed 2 h after the treadmill session, Fos expression was observed in the medial region of the rostral and central striatum, and in the dorsal region of the caudal striatum. Fos expression was prevented by pretreatment with the non-competitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist MK-801 (0.1 mg/kg) or the D1 dopamine receptor antagonist SCH-23390 (0.1 mg/kg), but not by pretreatment with the D2 receptor antagonist eticlopride (0.5 mg/kg). Thirty-six hours after 6-hydroxydopamine lesion, a considerable reduction in treadmill-induced Fos expression was observed in both sides; however, Fos expression in the lesioned striatum was higher than in the contralateral intact striatum. Several weeks after unilateral 6-hydroxydopamine lesion of the nigrostriatal system, treadmill-induced Fos expression was significantly, but not totally, reduced in the lesioned striatum. Corticostriatal deafferentation also led to considerable reduction in treadmill-induced Fos expression. The present results indicate that exercise induces striatal Fos expression and that, under physiological stimulation, concurrent activation of D1 and NMDA receptors is necessary for such expression to occur. Reduction of Fos expression is practically absolute after acute blockage of these receptors, but not after lesions, possibly due partially to compensatory changes.

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“…Second, induction of gene expression in NS neurons by amphetamine, as well as other pharmacological and electrophysiological manipulations, depends on activation of postsynaptic D1 and NMDA receptors. These two receptor systems interact at the intracellular level, probably through cAMP-PKA-dependent phosphorylation [Das et al, 1997;Konradi et al, 1996;Liste et al, 1995].…”

Section: Da Signal-to-noise Ratio and Synaptic Plasticitymentioning

confidence: 99%

Dopamine and N-Methyl-D- Aspartate Receptor Interactions in the Neostriatum

Cepeda

Levine²

1998

Dev Neurosci

318

173

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This review examines dopamine (DA) and glutamate receptor interactions in the neostriatum (NS) primarily from a neurophysiological perspective. Historically, a clear understanding of the function of DA in the NS has been difficult because it was considered a classical neurotransmitter with either excitatory or inhibitory actions and because many of the data were obtained by use of varying methodologies. When DA is considered a neuromodulator whose role is to alter how NS cells respond to glutamatergic inputs, many of its actions can be accounted for and predicted with great accuracy within a model of receptor subtype. In this model, DA via activation of D1 receptors potentiates responses mediated by activation of N-methyl-D-aspartate (NMDA) receptors. DA via activation of D2 receptors attenuates responses mediated by activation of non-NMDA receptors. Outcomes of combinations of NMDA and D2 and non-NMDA and D1 receptors are not as predictable. The mechanisms underlying the D1-NMDA receptor interactions appear to involve alterations in cell excitability mediated by activation of Ca²⁺ conductances and/or phosphorylation of NMDA receptors. Less is known about mechanisms underlying the D2-non-NMDA receptor interaction. The functional implications of this model in setting membrane potentials, signal-to-noise ratio, plasticity and excitotoxicity are discussed.

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Cortical stimulation induces Fos expression in striatal neurons via NMDA glutamate and dopamine receptors

Cited by 54 publications

References 69 publications

Context modulates the expression of conditioned motor sensitization, cellular activation and synaptophysin immunoreactivity

Context modulates the expression of conditioned motor sensitization, cellular activation and synaptophysin immunoreactivity

Treadmill running induces striatal Fos expression via NMDA glutamate and dopamine receptors

Dopamine and N-Methyl-D- Aspartate Receptor Interactions in the Neostriatum

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