2-Guanidinoethanol increased dopamine release and 3,4-dihydroxyphenylacetic acid content, but not homovanillic acid content in the rat brain

Electroneurochemical and enzymological studies

Isao Yokoi, Hideaki Kabuto, Katsuhisa Hukuyama, Yutaka Nishijima, Takehiko Ito, Katsumi Yufu, Kenji Akiyama, Akitane Mori

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The effects of 2-guanidinoethanol (GEt) on the release of monoamines and on the activity of their degrading enzymes were studied in order to investigate why 3,4-dihydroxyphenylacetic acid (DOPAC) increased to a much greater extent than homovanillic acid (HVA) after GEt injection into rat brain. In differential pulse voltammograms recorded using an electrochemically treated carbon fiber electrode, two distinct oxidation peaks, one at 130mV (DOPAC peak) and the other at 300 mV (5-hydroxyindoleacetic acid (5-HIAA) peak), were observed. In the hippocampus, the DOPAC peak increased markedly compared to the peak height recorded prior to the intracerebroventricular injection of GEt (6μmol). Although the DOPAC peak height increased to 350% 4 hours after GEt injection, the 5-HIAA peak showed no change. In the striatum, the DOPAC peak increased to 150% 3 hours after GEt injection. Serial changes in the extracellular levels of DOPAC, HVA, and 5-HIAA were monitored in the striatum after GEt injection, using an in vivo brain micro-dialysis technique. Although the DOPAC levels strated to increase 80 minutes after GEt injection, HVA and 5-HIAA levels showed no change. On the other hand, monoamineoxidase, which metabolizes dopamine to DOPAC, was not activated and catechol-0-methyltransferase, which metabolizes DOPAC to HVA, were not inhibited by 5 mM of GEt in vitro. These data suggested that GEt increased the release of dopamine, but not of serotonin, and that GEt might restrict the DOPAC transport system.

Original languageEnglish
Pages (from-to)735-740
Number of pages6
JournalNeurochemical Research
Volume17
Issue number7
DOIs
Publication statusPublished - Jul 1992

Fingerprint

3,4-Dihydroxyphenylacetic Acid
Homovanillic Acid
Rats
Dopamine
Brain
Acids
Hydroxyindoleacetic Acid
Injections
2-guanidinoethanol
Catechol O-Methyltransferase
Methyltransferases
Dialysis
Hippocampus
Serotonin
Electrodes

Keywords

  • 2-Guanidinoethanol
  • brain micro-dialysis
  • catechol-0-methyltransferase
  • in vivo voltammetry
  • monoamine release
  • monoamineoxidase

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry

Cite this

2-Guanidinoethanol increased dopamine release and 3,4-dihydroxyphenylacetic acid content, but not homovanillic acid content in the rat brain : Electroneurochemical and enzymological studies. / Yokoi, Isao; Kabuto, Hideaki; Hukuyama, Katsuhisa; Nishijima, Yutaka; Ito, Takehiko; Yufu, Katsumi; Akiyama, Kenji; Mori, Akitane.

In: Neurochemical Research, Vol. 17, No. 7, 07.1992, p. 735-740.

Research output: Contribution to journalArticle

Yokoi, Isao ; Kabuto, Hideaki ; Hukuyama, Katsuhisa ; Nishijima, Yutaka ; Ito, Takehiko ; Yufu, Katsumi ; Akiyama, Kenji ; Mori, Akitane. / 2-Guanidinoethanol increased dopamine release and 3,4-dihydroxyphenylacetic acid content, but not homovanillic acid content in the rat brain : Electroneurochemical and enzymological studies. In: Neurochemical Research. 1992 ; Vol. 17, No. 7. pp. 735-740.
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abstract = "The effects of 2-guanidinoethanol (GEt) on the release of monoamines and on the activity of their degrading enzymes were studied in order to investigate why 3,4-dihydroxyphenylacetic acid (DOPAC) increased to a much greater extent than homovanillic acid (HVA) after GEt injection into rat brain. In differential pulse voltammograms recorded using an electrochemically treated carbon fiber electrode, two distinct oxidation peaks, one at 130mV (DOPAC peak) and the other at 300 mV (5-hydroxyindoleacetic acid (5-HIAA) peak), were observed. In the hippocampus, the DOPAC peak increased markedly compared to the peak height recorded prior to the intracerebroventricular injection of GEt (6μmol). Although the DOPAC peak height increased to 350{\%} 4 hours after GEt injection, the 5-HIAA peak showed no change. In the striatum, the DOPAC peak increased to 150{\%} 3 hours after GEt injection. Serial changes in the extracellular levels of DOPAC, HVA, and 5-HIAA were monitored in the striatum after GEt injection, using an in vivo brain micro-dialysis technique. Although the DOPAC levels strated to increase 80 minutes after GEt injection, HVA and 5-HIAA levels showed no change. On the other hand, monoamineoxidase, which metabolizes dopamine to DOPAC, was not activated and catechol-0-methyltransferase, which metabolizes DOPAC to HVA, were not inhibited by 5 mM of GEt in vitro. These data suggested that GEt increased the release of dopamine, but not of serotonin, and that GEt might restrict the DOPAC transport system.",
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T1 - 2-Guanidinoethanol increased dopamine release and 3,4-dihydroxyphenylacetic acid content, but not homovanillic acid content in the rat brain

T2 - Electroneurochemical and enzymological studies

AU - Yokoi, Isao

AU - Kabuto, Hideaki

AU - Hukuyama, Katsuhisa

AU - Nishijima, Yutaka

AU - Ito, Takehiko

AU - Yufu, Katsumi

AU - Akiyama, Kenji

AU - Mori, Akitane

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Y1 - 1992/7

N2 - The effects of 2-guanidinoethanol (GEt) on the release of monoamines and on the activity of their degrading enzymes were studied in order to investigate why 3,4-dihydroxyphenylacetic acid (DOPAC) increased to a much greater extent than homovanillic acid (HVA) after GEt injection into rat brain. In differential pulse voltammograms recorded using an electrochemically treated carbon fiber electrode, two distinct oxidation peaks, one at 130mV (DOPAC peak) and the other at 300 mV (5-hydroxyindoleacetic acid (5-HIAA) peak), were observed. In the hippocampus, the DOPAC peak increased markedly compared to the peak height recorded prior to the intracerebroventricular injection of GEt (6μmol). Although the DOPAC peak height increased to 350% 4 hours after GEt injection, the 5-HIAA peak showed no change. In the striatum, the DOPAC peak increased to 150% 3 hours after GEt injection. Serial changes in the extracellular levels of DOPAC, HVA, and 5-HIAA were monitored in the striatum after GEt injection, using an in vivo brain micro-dialysis technique. Although the DOPAC levels strated to increase 80 minutes after GEt injection, HVA and 5-HIAA levels showed no change. On the other hand, monoamineoxidase, which metabolizes dopamine to DOPAC, was not activated and catechol-0-methyltransferase, which metabolizes DOPAC to HVA, were not inhibited by 5 mM of GEt in vitro. These data suggested that GEt increased the release of dopamine, but not of serotonin, and that GEt might restrict the DOPAC transport system.

AB - The effects of 2-guanidinoethanol (GEt) on the release of monoamines and on the activity of their degrading enzymes were studied in order to investigate why 3,4-dihydroxyphenylacetic acid (DOPAC) increased to a much greater extent than homovanillic acid (HVA) after GEt injection into rat brain. In differential pulse voltammograms recorded using an electrochemically treated carbon fiber electrode, two distinct oxidation peaks, one at 130mV (DOPAC peak) and the other at 300 mV (5-hydroxyindoleacetic acid (5-HIAA) peak), were observed. In the hippocampus, the DOPAC peak increased markedly compared to the peak height recorded prior to the intracerebroventricular injection of GEt (6μmol). Although the DOPAC peak height increased to 350% 4 hours after GEt injection, the 5-HIAA peak showed no change. In the striatum, the DOPAC peak increased to 150% 3 hours after GEt injection. Serial changes in the extracellular levels of DOPAC, HVA, and 5-HIAA were monitored in the striatum after GEt injection, using an in vivo brain micro-dialysis technique. Although the DOPAC levels strated to increase 80 minutes after GEt injection, HVA and 5-HIAA levels showed no change. On the other hand, monoamineoxidase, which metabolizes dopamine to DOPAC, was not activated and catechol-0-methyltransferase, which metabolizes DOPAC to HVA, were not inhibited by 5 mM of GEt in vitro. These data suggested that GEt increased the release of dopamine, but not of serotonin, and that GEt might restrict the DOPAC transport system.

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