Opposite effects of NMDA and AMPA receptor blockade on catalepsy induced by dopamine receptor antagonists

Papa, Stella M.; Engber, Thomas M.; Boldry, Robert C.; Chase, Thomas N.

doi:10.1016/0014-2999(93)90781-c

Cited by 54 publications

(24 citation statements)

References 20 publications

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“…The finding that GYKI 52466 does not alter spontaneous locomotor activity is in line with recent studies showing that single administration of AMPA antagonists does not enhance or even dose-dependently reduces motor activity in rodents (Klockgether et al, 1991;L6schmann et al, 1991;Hauber and Andersen, 1993;Papa et al, 1993;Starr and Starr, 1993;Browne and McCulloch, 1994). Our neurochemical data provide the first evidence that systemic administration of a low, but behaviourally active dose of GYKI 52466 does not affect DA metabolism in the forebrain.…”

Section: Discussionsupporting

confidence: 92%

“…Like NMDA antagonists, AMPA antagonists are cerebroprotective and anticonvulsant (for review see Rogawski, 1993). However, in some behavioural models in which NMDA antagonists produce motor stimulation and antagonize neuroleptic-induced catalepsy (Schmidt and Bubser, 1989;Carlsson and Carlsson, 1990) AMPA antagonists are ineffective: AMPA antagonists fail to stimulate locomotion in naive rats (Hauber and Andersen, 1993) and in reserpine-treated mice (Starr and Starr, 1993) and they do not reverse (Zadow and Schmidt, 1994) or even increase neuroleptic-induced catalepsy (Papa et al, 1993). The neurochemical actions underlying these differential effects of NMDA and AMPA antagonists are largely unknown.…”

Section: Introductionmentioning

confidence: 97%

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Behavioural and neurochemical interactions of the AMPA antagonist GYKI 52466 and the non-competitive NMDA antagonist dizocilpine in rats

Bubser

Tzschentke

Hauber

1995

J. Neural Transmission

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The behavioural and neurochemical effects of the N-methyl-D-aspartate (NMDA) antagonist dizocilpine and the alpha-amino-3-hydroxy-5-methylisoxazole- 4-propionic acid (AMPA) antagonist GYKI 52466, given alone or in combination, were investigated in rats. Locomotor activity was increased by dizocilpine (0.2 mg/kg), but not by GYKI 52466 (2.4 mg/kg). Dizocilpine-induced hyperlocomotion was reduced by co-administration of GYKI 52466. In dizocilpine-treated rats dopamine (DA) metabolism (measured as DOPAC [dihydroxyphenylacetic acid] or DOPAC/DA in post mortem brain tissue) was increased in the prefrontal cortex and nucleus accumbens. In GYKI 52466-treated rats serotonin was reduced in the prefrontal cortex and nucleus accumbens while DA metabolism was not affected. In rats treated with dizocilpine plus GYKI 52466, DA metabolism was increased only in the prefrontal cortex, but not in the nucleus accumbens, when compared with vehicle-treated animals. These data confirm that AMPA and NMDA antagonists do not have synergistic effects on locomotor activity. A differential role of NMDA and AMPA antagonists in the control of mesolimbic DA neurons will be discussed here.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 97%

Behavioural and neurochemical interactions of the AMPA antagonist GYKI 52466 and the non-competitive NMDA antagonist dizocilpine in rats

Bubser

Tzschentke

Hauber

1995

J. Neural Transmission

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“…In rats with unilateral nigral 6-hydroxydopamine lesions or MPTPtreated monkeys, systemic administration of NBQX reduced rotational behaviour and locomotor activity (LOschmann et al 1991). In addition, NBQX did not improve akinesia, but suppressed muscular rigidity in monoamine-depleted rats (Klockgether et al 1991) and did not antagonize raclopride-induced catalepsy (Papa et al 1993). These findings are congruent with the present data showing that GYKI given alone did not antagonize haloperidol-induced catalepsy.…”

Section: Discussionsupporting

confidence: 88%

The non-NMDA glutamate receptor antagonist GYKI 52466 counteracts locomotor stimulation and anticataleptic activity induced by the NMDA antagonist dizocilpine

Hauber

Andersen

1993

Naunyn-Schmiedeberg's Arch Pharmacol

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Summary.The effects of the non-NMDA glutamate receptor antagonist GYKI 52466 (2.4 and 4.8 mg/kg, i.p.) on spontaneous locomotor activity and haloperidol-induced catalepsy (0.5 mg/kg, i.p.) were assessed in naive rats and in rats pretreated with the NMDA antagonist dizocilpine (0.08 mg/kg, i.p.). GYKI 52466 given alone did not alter locomotor activity and haloperidol-induced catalepsy, but significantly antagonized the dizocilpineinduced locomotor stimulation and counteracted the anti-cataleptic effects of dizocilpine on haloperidol-induced catalepsy. Thus blockade of non-NMDA glutamate receptors antagonized the behavioural stimulant effects of a NMDA receptor blockade.

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“…In animal models of Parkinson's disease, antagonists of NMDA receptors substantially potentiate the short-term therapeutic effect of dopaminergic agents (Klockgether and Turski, 1990;Morelli et al, 1992;Papa et al, 1993;Kaur and Starr, 1997) and are effective in attenuating the abnormal motor behaviors produced by chronic dopaminergic treatment (Papa et al, 1995;Marin et al, 1996;Blanchet et al, 1997). Recent evidence suggests that the basis for the development of these abnormal motor behaviors may be that long-term treatment with dopaminergic agents modifies the properties of striatal NMDA receptors (Engber et al, 1994;Papa et al, 1995;Marin et al, 1996;Papa and Chase, 1996;Chase et al, 1998).…”

Section: Abstract: Glutamate Receptor; Nmda Receptor; Dopamine Recepmentioning

confidence: 99%

Dopamine D1 Receptor-Dependent Trafficking of Striatal NMDA Glutamate Receptors to the Postsynaptic Membrane

2001

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Recent work has shown substantial alterations in NMDA receptor subunit expression, assembly, and phosphorylation in the dopamine-depleted striatum of a rodent 6-hydroxydopamine model of Parkinson's disease. These modifications are hypothesized to result from the trafficking of NMDA receptors between subcellular compartments. Here we show that in rat striatal tissues the NR2A and NR2B subunits in the synaptosomal membrane, and not those in the light membrane and synaptic vesicle-enriched compartments, are tyrosine phosphorylated. The dopamine D1 receptor agonist SKF-82958 produces (1) an increase in NR1, NR2A, and NR2B proteins in the synaptosomal membrane fraction; (2) a decrease in NR1, NR2A, and NR2B proteins in the light membrane and synaptic vesicleenriched fractions; and (3) an increase in the tyrosine phosphorylation of NR2A and NR2B in the synaptosomal membrane compartment. The protein phosphatase inhibitor pervanadate reproduces the alterations in subcellular distribution and phosphorylation, whereas the effects of the dopamine D1 receptor agonist are blocked by genistein, a protein tyrosine kinase inhibitor. Dopamine D1 receptor agonist treatment does not change the subcellular distribution of the AMPA receptor subunits GluR1 or GluR2/3 in the striatum and has no effect on cortical or cerebellar NMDA receptor subunits. These data reveal a rapid dopamine D1 receptor-and tyrosine kinasedependent trafficking of striatal NMDA receptors between intracellular and postsynaptic sites. The subcellular trafficking of striatal NMDA receptors may play a significant role both in the pathogenesis of Parkinson's disease and in the development of adverse effects of chronic dopaminergic therapy in parkinsonian patients.

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Opposite effects of NMDA and AMPA receptor blockade on catalepsy induced by dopamine receptor antagonists

Cited by 54 publications

References 20 publications

Behavioural and neurochemical interactions of the AMPA antagonist GYKI 52466 and the non-competitive NMDA antagonist dizocilpine in rats

Behavioural and neurochemical interactions of the AMPA antagonist GYKI 52466 and the non-competitive NMDA antagonist dizocilpine in rats

The non-NMDA glutamate receptor antagonist GYKI 52466 counteracts locomotor stimulation and anticataleptic activity induced by the NMDA antagonist dizocilpine

Dopamine D1 Receptor-Dependent Trafficking of Striatal NMDA Glutamate Receptors to the Postsynaptic Membrane

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