NMDA receptor mediates dopamine release in the striatum of unanesthetized rats as measured by brain microdialysis

Martínez‐Fong, Daniel; Rosales, Manuel G.; Góngora-Alfaro, José L.; Hernández, Salvador Villalpando; Aceves, Gorge

doi:10.1016/0006-8993(92)91065-m

Cited by 84 publications

(33 citation statements)

References 45 publications

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“…This series circuit is consistent with the presence of , opiate receptors in substantia nigra and their absence on DAergic terminals in striatum (60). Moreover, corticostriatal fibers synapse on DAergic fibers, and blockade of the NMDA receptor may modulate DA release in striatum with certain stimuli (67,69).…”

Section: Discussionsupporting

confidence: 79%

“…Morphine activation of tt receptors on GABAergic neurons in substantia nigra pars reticulata has been suggested to decrease GABA release onto nigral DA neurons (1) resulting in increased DA neuronal activity (19,22) and release of DA in striatum (1,4,20). The DA release is modulated by NMDA receptors that could be located on presynaptic terminals or cell bodies of DA neurons (65)(66)(67)(68). The DA acts on striatal neurons with D1 receptors to induce c-fos and junB via mechanisms discussed below.…”

Section: Discussionmentioning

confidence: 99%

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

Liu

Nickolenko

Sharp

1994

Proc. Natl. Acad. Sci. U.S.A.

165

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Morphine induced the c-fos and junB immediate early genes in neurons of the medial and ventral striatn and nucleus accumbens. Induction of c-fos and junB mRNA and Fos protein was blocked by naloxone, the D1 dopamine (DA) receptor antagonists SCH23390 and SCH39166, and the N-methyl-D-aspartate (NMDA) glutamate receptor antagonist MK801. SCH23390 attenuated morphine induction of AP-1 binding in striatum, suggesting that c-fos andjunB contribute to AP-1 binding. SCH23390 and MK801 did not block morphine induction of c-fos and junB in septum. Since the morphine induction of c-fos and junE in striatum and nucleus accumbens (NA) was similar to that observed with cocaine and amphetamine, these data support current concepts that limbic striatum and NA are among the brain regions that mediate drug abuse. Furthermore, since DA and NMDA receptors may mediate opiate reward and opiate induction of c-fos andjunE, the DA/NMDA regulation of c-fos and junB and their target genes may produce long-term changes in the striatal and NA circuits that contribute to opiate drug abuse.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

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

Liu

Nickolenko

Sharp

1994

Proc. Natl. Acad. Sci. U.S.A.

165

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“…Although glycine is known as a major inhibitory neurotransmitter, glycine combines with the glycine binding site of the NMDA receptor and enhances excitatory neurotransmission (Xu et al 1999;Kuhse et al 1995;Nong et al 2003). Glycine enhanced NMDA evoked dopamine release, and 7-chloro-kynurenate, an NMDA antagonist, acting on a glycine site, markedly reduced this response (Martinez et al 1992); however, 5,7-DCKA injection did not prevent the increase of dopamine concentration by theanine injection in this study. These results suggested that theanine-increased glycine influenced interstitial dopamine via glycine receptors, and not NMDA receptors.…”

Section: Discussioncontrasting

confidence: 77%

Theanine, γ-glutamylethylamide, a unique amino acid in tea leaves, modulates neurotransmitter concentrations in the brain striatum interstitium in conscious rats

et al. 2008

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Theanine (c-glutamylethylamide) is one of the major amino acid components in green tea and can pass through the blood-brain barrier. Recent studies suggest that theanine affects the mammalian central nervous system; however, the detailed mechanism remains unclear. In this study, we demonstrated the effect of theanine on neurotransmission in the brain striatum by in vivo brain microdialysis. Theanine injection into the rat brain striatum did not increase the concentration of excitatory neurotransmitters in the perfusate. On the other hand, theanine injection increased the concentration of glycine in the perfusate. Because it has been reported that theanine promotes dopamine release in the rat striatum, we investigated the glycine and dopamine concentrations in the perfusate. Co-injection of glycine receptor antagonist, strychnine, reduced theanine-induced changes in dopamine. Moreover, AMPA receptor antagonist, which regulates glycine and GABA release from glia cells, inhibited these effects of theanine and this result was in agreement with the known inhibitory effect of theanine at AMPA receptors.

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“…NMDA receptors may be located presynaptically on dopamine terminals and modulate dopamine release in striatum (Leviel et al, 1990;Krebs et al, 1991;Wang, 1991;Martinez-Fong et al, 1992). M K 801 could block presynaptic NMDA receptors on striatal / NAc dopamine terminals, block dopamine release normally produced by morphine, and prevent Fos induction.…”

Section: Coactivation Of D 1 and Nmda Receptors Mediates Induction Ofmentioning

confidence: 99%

Systemic Morphine-Induced Fos Protein in the Rat Striatum and Nucleus Accumbens Is Regulated by μ Opioid Receptors in the Substantia Nigra and Ventral Tegmental Area

1997

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To characterize how systemic morphine induces Fos protein in dorsomedial striatum and nucleus accumbens (NAc), we examined the role of receptors in striatum, substantia nigra (SN), and ventral tegmental area (VTA). Morphine injected into medial SN or into VTA of awake rats induced Fos in neurons in ipsilateral dorsomedial striatum and NAc. Morphine injected into lateral SN induced Fos in dorsolateral striatum and globus pallidus. Fos induction in dorsomedial striatum and NAc after systemic administration of morphine seems to be mediated by dopamine neurons in medial SN and VTA that project to medial striatum and NAc, respectively. Systemic morphine is proposed to act on opioid receptors located on GABAergic interneurons in medial SN and VTA. Inhibition of these GABA interneurons disinhibits medial SN and VTA dopamine neurons, producing dopamine release in medial striatum and NAc. This activates D 1 dopamine receptors and coupled with the coactivation of NMDA receptors possibly from cortical glutamate input induces Fos in striatal and NAc neurons. The modulation of target gene expression by Fos could influence addictive behavioral responses to opiates. The c-fos and junB immediate early genes (I EGs) are induced in striatum and nucleus accumbens (NAc) after systemic administration of cocaine and amphetamine (Graybiel et al

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NMDA receptor mediates dopamine release in the striatum of unanesthetized rats as measured by brain microdialysis

Cited by 84 publications

References 45 publications

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

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

Theanine, γ-glutamylethylamide, a unique amino acid in tea leaves, modulates neurotransmitter concentrations in the brain striatum interstitium in conscious rats

Systemic Morphine-Induced Fos Protein in the Rat Striatum and Nucleus Accumbens Is Regulated by μ Opioid Receptors in the Substantia Nigra and Ventral Tegmental Area

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