Effects of N-methyl-D-aspartate, kainate or veratridine on extracellular concentrations of free D-serine and L-glutamate in rat striatum: an in vivo microdialysis study

Hashimoto, Atsushi; Kanda, Jun; Oka, Tetsuo

doi:10.1016/s0361-9230(00)00357-9

Cited by 32 publications

(25 citation statements)

References 39 publications

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“…KA is usually effective at concentrations as low as 1 mM. The high KA concentration required here and in previous studies [18][19][20] to observe a significant effect further weakens the hypothesis that it is a traditional AMPA/KA receptor that mediates D-serine release from astrocytes.…”

contrasting

confidence: 40%

“…In cultured astrocytes, activation of a-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)/kainic acid (KA) receptors induces D-serine efflux giving rise to the hypothesis that presynaptic neurons release glutamate, which in turn activates AMPA/KA receptors on neighboring astrocytes, initiating D-serine release [18,19]. Unfortunately, application of KA in vivo has not produced similar results [20]. Alternatively, physiological concentrations of L-serine have been shown to induce D-serine efflux from cultured astrocytes in a manner consistent with system ASC transporters (ASCT), suggesting that these transporters play a role in regulating D-serine levels in the extracellular space [21].…”

Section: Introductionmentioning

confidence: 99%

“…In vitro studies using astrocyte cultures are relatively straightforward but do not always reflect in vivo activity. Hashimoto [20] has performed microdialysis sampling followed by an enantiomeric HPLC separation to analyze D-serine dynamics in the rat brain but the sampling rate was limited to once every 20 min. We have developed an online microdialysis-CE (MD-CE) assay for D-serine that improved the sampling rate to once every 10-20 s, much more suitable for measuring neuromessenger dynamics [22].…”

Section: Introductionmentioning

confidence: 99%

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MeasuringD-serine efflux from mouse cortical brain slices using online microdialysis-capillary electrophoresis

O'Brien

Bowser

2006

Electrophoresis

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Efflux of a number of important neurochemicals, including D-serine, L-serine, taurine, glutamate, and gamma-aminobutyric acid (GABA), from mouse cortical brain slices housed in a 7 microL perfusion chamber was monitored using online microdialysis-CE (MD-CE). Analyte concentrations could be measured every 20-27 s using the MD-CE instrument. Stimulation with high potassium induced increased release of D-serine. Kainic acid (KA) induced D-serine release, but this release was not blocked by 6-cyano-7-nitroquinoxaline-2,3-dione, suggesting that alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid/KA receptors do not mediate D-serine release. Application of L-serine, the precursor of D-serine, resulted in increased extracellular D-serine concentrations. L-Cysteine also increased extracellular D-serine levels in a partially Na+-dependent manner. The observed effects upon application of L-serine and L-cysteine support the involvement of ASC neutral amino acid transporters in regulating the extracellular concentration of D-serine concentration through competitive inhibition of uptake or increased release through heteroexchange.

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contrasting

confidence: 40%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MeasuringD-serine efflux from mouse cortical brain slices using online microdialysis-capillary electrophoresis

O'Brien

Bowser

2006

Electrophoresis

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“…Also, it was reported that NAAG is only 10-fold more selective for mGluR3 than mGluR2 (Cartmell et al, 1998;Schweitzer et al, 2000). Although NAAG may also acts as a weak NMDA agonist, the inhibitory effect of NAAG on glutamate release is unlikely mediated by activating NMDA receptors because previous studies have shown that NMDA receptor activation increases glutamate release in the striatum (Hashimoto et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Group II Metabotropic Glutamate Receptors Modulate Extracellular Glutamate in the Nucleus Accumbens

Xi¹,

Baker²,

Shen³

et al. 2002

J Pharmacol Exp Ther

196

157

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The regulation of extracellular glutamate in the nucleus accumbens by group II metabotropic glutamate receptors (mGluR2/3) was examined in vivo. Stimulation of mGluR2/3 with 2R,4R-4-aminopyrrolidine-2,4-dicarboxylate (APDC) or N-acetylaspartylglutamate reduced extracellular glutamate levels. Conversely, blockade of mGluR2/3 by LY143495 or (RS)-1-amino-5-phosphonoindan-1-carboxylic acid (APICA) increased extracellular glutamate, an effect antagonized by the coadministration of APDC. These effects likely involve both vesicular and nonvesicular glutamate, because the increase in glutamate by APICA or the decrease by APDC was prevented by blocking N-type calcium channels and the release of glutamate after potassium-induced membrane depolarization was antagonized by APDC. In addition, blockade of the cystine-glutamate exchange, a major nonvesicular source of extracellular glutamate, by (S)-4-carboxyphenylglycine blocked the effects induced by either APDC or APICA. However, blockade of Na ϩ channels by tetrodotoxin or Na ϩ -dependent glutamate transporters by DL-threo-␤-benzyloxyaspartate failed to affect the alterations in extracellular glutamate by APICA or APDC, respectively. Group II mGluRs are G i -coupled and coperfusion with the cAMP-dependent protein kinase (PKA) activator Sp-cAMPS blocked the reduction in glutamate by APDC and the PKA inhibitor Rp-cAMPS prevented the elevation in glutamate by APICA. Taken together, these data support three conclusions: 1) group II mGluRs regulate both vesicular and nonvesicular release of glutamate in the nucleus accumbens, 2) there is tonic in vivo stimulation of mGluR2/3 by endogenous glutamate, and 3) modulation of group II mGluRs of extracellular glutamate is Ca 2ϩ -and PKAdependent.

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“…Transporter-mediated exchange with other neutral amino acids may be among important mechanisms contributing to the efflux of D-serine because L-serine and Lthreonine are potent inducers of D-serine efflux from cultured astrocytes, being more effective than kainate (Ribeiro et al, 2002). Also noteworthy are the findings of Hashimoto et al (2000), who demonstrated that intrastriatal perfusion of NMDA or kainate caused a significant decrease, rather than an increase, in extracellular concentrations of D-serine. Clearly, there remains much to be done for elucidation of the mechanisms regulating extracellular levels of D-serine.…”

Section: Discussionmentioning

confidence: 99%

Endogenous d-Serine Is Involved in Induction of Neuronal Death by N-Methyl-d-aspartate and Simulated Ischemia in Rat Cerebrocortical Slices

Katsuki¹,

Nonaka²,

Shirakawa³

et al. 2004

J Pharmacol Exp Ther

103

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Emerging evidence indicates that D-serine rather than glycine serves as an endogenous agonist at glycine site of the Nmethyl-D-aspartate (NMDA) subtype of glutamate receptors, in several nervous tissues, including the developing cerebellum and the retina. Here, we examined whether endogenous Dserine plays a significant role in neuronal damage resulting from excitotoxic insults in the cerebral cortex, using rat brain slices maintained in a defined salt solution. Neuronal cell death induced by application of NMDA or by oxygen-glucose deprivation (simulated ischemia) was markedly suppressed by a competitive glycine site antagonist 2,7-dichlorokynurenic acid. Addition of glycine or D-serine did not augment neuronal damage by NMDA or simulated ischemia, indicating that sufficient amount of glycine site agonist(s) is supplied endogenously within the slices. Application of D-amino acid oxidase, an enzyme that degrades D-serine, markedly inhibited neuronal damage by NMDA and simulated ischemia, which was reversed by addition of excess D-serine or glycine. Sensitivity to the glycine site antagonist of NMDA-or ischemia-induced damage was not affected by the presence of a non-NMDA receptor antagonist, suggesting that kainate receptor-stimulated D-serine release as demonstrated in primary cultured astrocytes does not contribute significantly to the extent of neuronal injury in these settings. The present results suggest that endogenous supply of D-serine as a glycine site agonist is important for neuronal injury involving NMDA receptor overactivation in the cerebral cortex.

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Effects of N-methyl-D-aspartate, kainate or veratridine on extracellular concentrations of free D-serine and L-glutamate in rat striatum: an in vivo microdialysis study

Cited by 32 publications

References 39 publications

MeasuringD-serine efflux from mouse cortical brain slices using online microdialysis-capillary electrophoresis

MeasuringD-serine efflux from mouse cortical brain slices using online microdialysis-capillary electrophoresis

Group II Metabotropic Glutamate Receptors Modulate Extracellular Glutamate in the Nucleus Accumbens

Endogenous d-Serine Is Involved in Induction of Neuronal Death by N-Methyl-d-aspartate and Simulated Ischemia in Rat Cerebrocortical Slices

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