Correlation of in vivo nitric oxide and cGMP with glutamate/glutamine metabolism in the rat striatum

Kouichi Ohta, Nobuo Araki, Mamoru Shibata, Junichi Hamada, Satoru Komatsumoto, Kunio Shimazu, Yasuo Fukuuchi

研究成果: Article

13 引用 (Scopus)

抄録

We have examined how the suppression of endogenous production of nitric oxide (NO) in the striatal tissue affects release of glutamate (GLU) and glutamine (GLN) in pentobarbital-anesthetized male Sprague-Dawley rats. For the quantitative measurement of tissue NO production and amino acid release, an in vivo assay system for extracellular nitrite (NO2 -) and amino acids was employed using an in vivo microdialysis technique. An NO synthase inhibitor (N(G)-nitro-L-arginine methyl ester, L-NAME) in concentrations ranging between 4-40 mM was perfused into the rat striatum using the assay system. Tissue NO production was found to be inversely proportional to the L-NAME concentration. L-NAME likewise decreased striatal levels of GLU and GLN. Furthermore, tissue NO production showed a positive correlation with GLU (R = 0.62, P < 0.02) and GLN (R = 0.86, P < 0.001) concentrations. Exogenous application of NO and cGMP by intrastriatal perfusion with 0.1-2.5 mM hydroxylamine and 0.4-10 mM 8-bromo-cGMP, respectively, increased striatal GLU release in a dose-related manner. Hydroxylamine reduced GLN release, and 8-bromo-cGMP showed a tendency to decrease GLN. In conclusion, striatal GLU/GLN metabolism is a function of the tissue concentration of NO. Normal endogenous concentration of NO causes GLU to be released at a consistent basal level, and enhanced tissue NO production facilitates GLU release via pathways including cGMP formation. We hypothesize that NO may suppress GLN formation by astrocytes.

元の言語English
ページ(範囲)379-384
ページ数6
ジャーナルNeuroscience Research
25
発行部数4
DOI
出版物ステータスPublished - 1996 8

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Glutamine
Glutamic Acid
Nitric Oxide
Corpus Striatum
NG-Nitroarginine Methyl Ester
Hydroxylamine
Amino Acids
Microdialysis
Pentobarbital
Nitrites
Nitric Oxide Synthase
Astrocytes
Sprague Dawley Rats
Perfusion

ASJC Scopus subject areas

  • Neuroscience(all)

これを引用

Correlation of in vivo nitric oxide and cGMP with glutamate/glutamine metabolism in the rat striatum. / Ohta, Kouichi; Araki, Nobuo; Shibata, Mamoru; Hamada, Junichi; Komatsumoto, Satoru; Shimazu, Kunio; Fukuuchi, Yasuo.

:: Neuroscience Research, 巻 25, 番号 4, 08.1996, p. 379-384.

研究成果: Article

Ohta, Kouichi ; Araki, Nobuo ; Shibata, Mamoru ; Hamada, Junichi ; Komatsumoto, Satoru ; Shimazu, Kunio ; Fukuuchi, Yasuo. / Correlation of in vivo nitric oxide and cGMP with glutamate/glutamine metabolism in the rat striatum. :: Neuroscience Research. 1996 ; 巻 25, 番号 4. pp. 379-384.
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title = "Correlation of in vivo nitric oxide and cGMP with glutamate/glutamine metabolism in the rat striatum",
abstract = "We have examined how the suppression of endogenous production of nitric oxide (NO) in the striatal tissue affects release of glutamate (GLU) and glutamine (GLN) in pentobarbital-anesthetized male Sprague-Dawley rats. For the quantitative measurement of tissue NO production and amino acid release, an in vivo assay system for extracellular nitrite (NO2 -) and amino acids was employed using an in vivo microdialysis technique. An NO synthase inhibitor (N(G)-nitro-L-arginine methyl ester, L-NAME) in concentrations ranging between 4-40 mM was perfused into the rat striatum using the assay system. Tissue NO production was found to be inversely proportional to the L-NAME concentration. L-NAME likewise decreased striatal levels of GLU and GLN. Furthermore, tissue NO production showed a positive correlation with GLU (R = 0.62, P < 0.02) and GLN (R = 0.86, P < 0.001) concentrations. Exogenous application of NO and cGMP by intrastriatal perfusion with 0.1-2.5 mM hydroxylamine and 0.4-10 mM 8-bromo-cGMP, respectively, increased striatal GLU release in a dose-related manner. Hydroxylamine reduced GLN release, and 8-bromo-cGMP showed a tendency to decrease GLN. In conclusion, striatal GLU/GLN metabolism is a function of the tissue concentration of NO. Normal endogenous concentration of NO causes GLU to be released at a consistent basal level, and enhanced tissue NO production facilitates GLU release via pathways including cGMP formation. We hypothesize that NO may suppress GLN formation by astrocytes.",
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T1 - Correlation of in vivo nitric oxide and cGMP with glutamate/glutamine metabolism in the rat striatum

AU - Ohta, Kouichi

AU - Araki, Nobuo

AU - Shibata, Mamoru

AU - Hamada, Junichi

AU - Komatsumoto, Satoru

AU - Shimazu, Kunio

AU - Fukuuchi, Yasuo

PY - 1996/8

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N2 - We have examined how the suppression of endogenous production of nitric oxide (NO) in the striatal tissue affects release of glutamate (GLU) and glutamine (GLN) in pentobarbital-anesthetized male Sprague-Dawley rats. For the quantitative measurement of tissue NO production and amino acid release, an in vivo assay system for extracellular nitrite (NO2 -) and amino acids was employed using an in vivo microdialysis technique. An NO synthase inhibitor (N(G)-nitro-L-arginine methyl ester, L-NAME) in concentrations ranging between 4-40 mM was perfused into the rat striatum using the assay system. Tissue NO production was found to be inversely proportional to the L-NAME concentration. L-NAME likewise decreased striatal levels of GLU and GLN. Furthermore, tissue NO production showed a positive correlation with GLU (R = 0.62, P < 0.02) and GLN (R = 0.86, P < 0.001) concentrations. Exogenous application of NO and cGMP by intrastriatal perfusion with 0.1-2.5 mM hydroxylamine and 0.4-10 mM 8-bromo-cGMP, respectively, increased striatal GLU release in a dose-related manner. Hydroxylamine reduced GLN release, and 8-bromo-cGMP showed a tendency to decrease GLN. In conclusion, striatal GLU/GLN metabolism is a function of the tissue concentration of NO. Normal endogenous concentration of NO causes GLU to be released at a consistent basal level, and enhanced tissue NO production facilitates GLU release via pathways including cGMP formation. We hypothesize that NO may suppress GLN formation by astrocytes.

AB - We have examined how the suppression of endogenous production of nitric oxide (NO) in the striatal tissue affects release of glutamate (GLU) and glutamine (GLN) in pentobarbital-anesthetized male Sprague-Dawley rats. For the quantitative measurement of tissue NO production and amino acid release, an in vivo assay system for extracellular nitrite (NO2 -) and amino acids was employed using an in vivo microdialysis technique. An NO synthase inhibitor (N(G)-nitro-L-arginine methyl ester, L-NAME) in concentrations ranging between 4-40 mM was perfused into the rat striatum using the assay system. Tissue NO production was found to be inversely proportional to the L-NAME concentration. L-NAME likewise decreased striatal levels of GLU and GLN. Furthermore, tissue NO production showed a positive correlation with GLU (R = 0.62, P < 0.02) and GLN (R = 0.86, P < 0.001) concentrations. Exogenous application of NO and cGMP by intrastriatal perfusion with 0.1-2.5 mM hydroxylamine and 0.4-10 mM 8-bromo-cGMP, respectively, increased striatal GLU release in a dose-related manner. Hydroxylamine reduced GLN release, and 8-bromo-cGMP showed a tendency to decrease GLN. In conclusion, striatal GLU/GLN metabolism is a function of the tissue concentration of NO. Normal endogenous concentration of NO causes GLU to be released at a consistent basal level, and enhanced tissue NO production facilitates GLU release via pathways including cGMP formation. We hypothesize that NO may suppress GLN formation by astrocytes.

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KW - Glutamine synthase

KW - Hydroxylamine

KW - In vivo microdialysis

KW - N(G)-nitro-L-arginine methyl ester

KW - Neurotransmitter

KW - Nitric oxide synthase

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