Modulation of striatal [3H]-glutamic acid release by dopaminergic drugs

Mitchell, P. R.; Doggett, N.S.

doi:10.1016/0024-3205(80)90592-5

Cited by 168 publications

(44 citation statements)

References 20 publications

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“…This effect could be due to a disinhibition of corticostriatal glutamatergic transmission via antagonism of the D-2 receptor produced by the accumulation of haloperidol in the brain. Along these lines, it has been shown that there are D-2 receptors located on corticostriatal nerve terminals (Garau et al, 1978;Schwartz et al, 1978;Theodorou et al, 1981;Filloux et al, 1989) and that dopamine and D-2 agonists inhibit stimulated glutamate efflux in the striaturn (Mitchell and Doggett, 1980;Rowlands and Roberts, 1980;Nieoullon et al, 1982;Kerkerian and Nieoullon, 1988;Maura et al, 1988Maura et al, , 1989Yamamoto and Davy, 1992). Furthermore, chronic treatment with the D-2 antagonist (-)sulpiride increases glutamate in cerebrospinal fluid of rats (Kim et al, 1983).…”

Section: Discussionmentioning

confidence: 99%

“…There is increasing evidence, however, of an interaction between dopamine and the excitatory amino acid neurotransmitter glutamate. In particular, there is a substantial amount of anatomical and neurochemical evidence that dopamine can modulate corticostriatal glutamate efflux via the D-2 receptor (Garau et al, 1978;Schwartz et al, 1978;Mitchell and Doggett, 1980;Rowlands and Roberts, 1980;Theodorou et al, 198 1;Nieoullon et al, 1982;. Filloux et al, 1988;Kerkerian and Nieoullon, 1988;Maura et al, 1988Maura et al, , 1989Yamamoto and Davy, 1992).…”

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confidence: 99%

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Differential effects of chronic antipsychotic drug treatment on extracellular glutamate and dopamine concentrations

1994

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Typical and atypical antipsychotic drugs have been reported to affect basal dopaminergic activity differentially in nigrostriatal and limbic structures after acute and chronic administration in animals. In addition, glutamate has been implicated in the pathophysiology of schizophrenia. The purpose of this study was to examine basal and locally stimulated glutamate and dopamine efflux in the caudate, nucleus accumbens, and medial prefrontal cortex using in vivo microdialysis after chronic clozapine and haloperidol treatment. Basal extracellular concentrations of dopamine in the caudate and nucleus accumbens were not different between the drug treatment groups; however, dopamine concentrations were higher in the medial prefrontal cortex after chronic clozapine treatment. Depolarization-induced dopamine release with 80 mM K+ in all three brain regions was attenuated by haloperidol treatment. In contrast, basal concentrations of extracellular glutamate were markedly higher in the caudate and modestly increased in the nucleus accumbens but not in the prefrontal cortex after chronic haloperidol. Chronic clozapine treatment did not have an effect in any of the brain regions examined. K(+)-stimulated glutamate efflux was unaffected by haloperidol or clozapine in the caudate or prefrontal cortex; however, stimulated glutamate release in the nucleus accumbens was enhanced by clozapine. These data are suggestive of a depolarization inactivation of dopamine nerve terminals in striatum and cortex as revealed by an attenuation of local K(+)- induced stimulation of dopamine efflux. These results also provide new evidence for a role of glutamate in discriminating the neurochemical effects of chronic treatment with antipsychotic drugs.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Differential effects of chronic antipsychotic drug treatment on extracellular glutamate and dopamine concentrations

1994

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“…DA synapses are localized most frequently to the necks of spines and shafts of dendrites of NS spiny neurons postsynaptically [Freund et al, 1984], a position from which they would be capable of altering responses induced by activation of the glutamate-containing synapses localized on spine heads. Similarly, DA may have a modulatory role presynaptically since there is evidence that DA is capable of altering glutamate release, probably via D2 receptors [Kornhuber and Kornhuber, 1986;Mitchell and Doggett, 1980;Rowlands and Roberts, 1980;Yamamoto and Davy, 1992].…”

Section: Historical Perspective Of the Actions Of Da On Ns Neuronsmentioning

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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“…Several biochemical and pharmacological findings indicate the existence of inhibitory dopamine receptors localized on cerebral cortical afTerents to the rat striatum [4,9,11,13,14,[17][18][19], The cortico-striatal fibers are glutamatcrgic. The question of whether do paminergic inhibitory synapses exist on the glutamatergic terminals in the striatum is of interest for the theory of schizophrenia [10].…”

Section: Introductionmentioning

confidence: 99%

Axo-Axonic Synapses in the Rat Striatum

Kornhuber¹,

Kornhuber²

1983

Eur Neurol

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Inthe rat striatum axo-axonic synapses are seen relatively rarely in individual sections. From topological data it is concluded that the real occurrence of these synapses is much higher than the apparent occurrence as judged from single sections. A mathematical consideration is given to account for the distance between the two synapses in series. Their possible role in the action of neuroleptic drugs and for the theory of schizophrenia has been postulated.

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Modulation of striatal [3H]-glutamic acid release by dopaminergic drugs

Cited by 168 publications

References 20 publications

Differential effects of chronic antipsychotic drug treatment on extracellular glutamate and dopamine concentrations

Differential effects of chronic antipsychotic drug treatment on extracellular glutamate and dopamine concentrations

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

Axo-Axonic Synapses in the Rat Striatum

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