Long-term enhancement of dopamine release by high frequency tetanic stimulation via aN-methyl-d-aspartate-receptor-mediated pathway in rat striatum

M. Ochi, H. Inoue, S. Koizumi, Shigenobu Shibata, S. Watanabe

Research output: Contribution to journalArticle

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Abstract

We studied the effects of high frequency tetanic stimulation of the striatum on the KCl (20 mM)-evoked dopamine release in rat striatal slices. The KCl-evoked dopamine release was potentiated by high frequency tetanic stimulation (10-20 Hz) of the striatum including the corticostriatal fibers, and this potentiation was observed until 3 h after high frequency tetanic stimulation. Potentiation of dopamine release after high frequency tetanic stimulation was induced not only by KCl but also by glutamate in Mg2+-free medium,N-methyl-d-aspartate in Mg2+-free medium, and bydl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid. 2-amino-5-phosphovalerate, 3-[(±)-2-carboxypiperazine-4-yl]-propyl-1-phosphonate or dibenzocycloheptaneimine,N-methyl-d-aspartate receptor inhibitors, abolished enhancement by tetanus, whereas, 6,7-dinitroquinoxaline-2,3-dione, an antagonist ofdl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid ionotropic receptors, orl-2-amino-4-phosphonobutyrate, an antagonist of glutamate metabotropic receptors, showed no effect. Moreover, pretreatment with glutamate orN-methyl-d-aspartate in the absence of Mg2+ also facilitated dopamine release evoked by KCl concentrations. When extracellular Ca2+ was removed from the medium during pretreatment, potentiation by glutamate disappeared. We conclude that activation ofN-methyl-d-aspartate receptors on dopaminergic nerve terminals in the striatum produces the long-term changes in efficacy of the response to KCl or glutamatergic agents. That is, plastical phenomena could exist at presynaptic levels between glutamatergic neurons and dopaminergic neurons in striatum.

Original languageEnglish
Pages (from-to)29-36
Number of pages8
JournalNeuroscience
Volume66
Issue number1
DOIs
Publication statusPublished - 1995
Externally publishedYes

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Dopamine
Isoxazoles
Glutamic Acid
Aspartic Acid
Excitatory Amino Acid Agents
Corpus Striatum
Organophosphonates
Metabotropic Glutamate Receptors
Dopaminergic Neurons
Tetanus
Neurons
aspartic acid receptor
propionic acid

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Long-term enhancement of dopamine release by high frequency tetanic stimulation via aN-methyl-d-aspartate-receptor-mediated pathway in rat striatum. / Ochi, M.; Inoue, H.; Koizumi, S.; Shibata, Shigenobu; Watanabe, S.

In: Neuroscience, Vol. 66, No. 1, 1995, p. 29-36.

Research output: Contribution to journalArticle

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abstract = "We studied the effects of high frequency tetanic stimulation of the striatum on the KCl (20 mM)-evoked dopamine release in rat striatal slices. The KCl-evoked dopamine release was potentiated by high frequency tetanic stimulation (10-20 Hz) of the striatum including the corticostriatal fibers, and this potentiation was observed until 3 h after high frequency tetanic stimulation. Potentiation of dopamine release after high frequency tetanic stimulation was induced not only by KCl but also by glutamate in Mg2+-free medium,N-methyl-d-aspartate in Mg2+-free medium, and bydl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid. 2-amino-5-phosphovalerate, 3-[(±)-2-carboxypiperazine-4-yl]-propyl-1-phosphonate or dibenzocycloheptaneimine,N-methyl-d-aspartate receptor inhibitors, abolished enhancement by tetanus, whereas, 6,7-dinitroquinoxaline-2,3-dione, an antagonist ofdl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid ionotropic receptors, orl-2-amino-4-phosphonobutyrate, an antagonist of glutamate metabotropic receptors, showed no effect. Moreover, pretreatment with glutamate orN-methyl-d-aspartate in the absence of Mg2+ also facilitated dopamine release evoked by KCl concentrations. When extracellular Ca2+ was removed from the medium during pretreatment, potentiation by glutamate disappeared. We conclude that activation ofN-methyl-d-aspartate receptors on dopaminergic nerve terminals in the striatum produces the long-term changes in efficacy of the response to KCl or glutamatergic agents. That is, plastical phenomena could exist at presynaptic levels between glutamatergic neurons and dopaminergic neurons in striatum.",
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AB - We studied the effects of high frequency tetanic stimulation of the striatum on the KCl (20 mM)-evoked dopamine release in rat striatal slices. The KCl-evoked dopamine release was potentiated by high frequency tetanic stimulation (10-20 Hz) of the striatum including the corticostriatal fibers, and this potentiation was observed until 3 h after high frequency tetanic stimulation. Potentiation of dopamine release after high frequency tetanic stimulation was induced not only by KCl but also by glutamate in Mg2+-free medium,N-methyl-d-aspartate in Mg2+-free medium, and bydl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid. 2-amino-5-phosphovalerate, 3-[(±)-2-carboxypiperazine-4-yl]-propyl-1-phosphonate or dibenzocycloheptaneimine,N-methyl-d-aspartate receptor inhibitors, abolished enhancement by tetanus, whereas, 6,7-dinitroquinoxaline-2,3-dione, an antagonist ofdl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid ionotropic receptors, orl-2-amino-4-phosphonobutyrate, an antagonist of glutamate metabotropic receptors, showed no effect. Moreover, pretreatment with glutamate orN-methyl-d-aspartate in the absence of Mg2+ also facilitated dopamine release evoked by KCl concentrations. When extracellular Ca2+ was removed from the medium during pretreatment, potentiation by glutamate disappeared. We conclude that activation ofN-methyl-d-aspartate receptors on dopaminergic nerve terminals in the striatum produces the long-term changes in efficacy of the response to KCl or glutamatergic agents. That is, plastical phenomena could exist at presynaptic levels between glutamatergic neurons and dopaminergic neurons in striatum.

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