Signaling pathways in the nitric oxide and iron-induced dopamine release in the striatum of freely moving rats: Role of extracellular Ca2+ and L-type Ca2+ channels

Gaia Rocchitta, Rossana Migheli, Maria P. Mura, Giuseppe Grella, Giovanni Esposito, Bianca Marchetti, Egidio Miele, Maria S. Desole, Maddalena Miele, Pier Andrea Serra

Research output: Contribution to journalArticle

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Abstract

We showed previously that exogenous iron potentiated nitric oxide (NO) donor-induced release of striatal dopamine (DA) in freely moving rats, using microdialysis. In this study, the increase in dialysate DA induced by intrastriatal infusion of the NO-donor 3-morpholinosydnonimine (SIN-1, 1.0 mM for 180 min) was scarcely affected by Ca2+ omission. N-methyl-d-glucamine dithiocarbamate (MGD) is a thiol compound whose NO trapping activity is potentiated by iron(II). Intrastriatal co-infusion of MGD either alone or associated with iron(II), however, potentiated SIN-1-induced increases in dialysate DA. In contrast, co-infusion of the NO trapper 4-(carboxyphenyl)-4, 4,5,5-tetramethylimidazole-1-oxyl 3-oxide (carboxy-PTIO) significantly attenuated the increase in dialysate DA induced by SIN-1 (5.0 mM for 180 min). SIN-1+MGD+iron(II)-induced increases in dialysate DA were inhibited by Ca 2+ omission or co-infusion of either deferoxamine or the L-type (Cav 1.1-1.3) Ca2+ channel inhibitor nifedipine; in contrast, the increase was scarcely affected by co-infusion of the N-type (Cav 2.2) Ca2+ channel inhibitor ω-conotoxin GVIA. These results demonstrate that exogenous NO-induced release of striatal DA is independent on extracellular Ca2+; however, in presence of the NO trapper MGD, NO may preferentially react with either endogenous or exogenous iron to form a complex which releases striatal DA with an extracellular Ca 2+-dependent and nifedipine-sensitive mechanism.

Original languageEnglish
Pages (from-to)18-29
Number of pages12
JournalBrain Research
Volume1047
Issue number1
DOIs
Publication statusPublished - Jun 14 2005

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Dopamine
Nitric Oxide
Iron
Dialysis Solutions
Corpus Striatum
Nitric Oxide Donors
Nifedipine
Conotoxins
Deferoxamine
Microdialysis
Sulfhydryl Compounds
Oxides

Keywords

  • Calcium channels
  • Complex
  • Exogenous nitric oxide
  • Iron
  • Parkinson's disease
  • Striatal dopamine release

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Signaling pathways in the nitric oxide and iron-induced dopamine release in the striatum of freely moving rats : Role of extracellular Ca2+ and L-type Ca2+ channels. / Rocchitta, Gaia; Migheli, Rossana; Mura, Maria P.; Grella, Giuseppe; Esposito, Giovanni; Marchetti, Bianca; Miele, Egidio; Desole, Maria S.; Miele, Maddalena; Serra, Pier Andrea.

In: Brain Research, Vol. 1047, No. 1, 14.06.2005, p. 18-29.

Research output: Contribution to journalArticle

Rocchitta, Gaia ; Migheli, Rossana ; Mura, Maria P. ; Grella, Giuseppe ; Esposito, Giovanni ; Marchetti, Bianca ; Miele, Egidio ; Desole, Maria S. ; Miele, Maddalena ; Serra, Pier Andrea. / Signaling pathways in the nitric oxide and iron-induced dopamine release in the striatum of freely moving rats : Role of extracellular Ca2+ and L-type Ca2+ channels. In: Brain Research. 2005 ; Vol. 1047, No. 1. pp. 18-29.
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AU - Migheli, Rossana

AU - Mura, Maria P.

AU - Grella, Giuseppe

AU - Esposito, Giovanni

AU - Marchetti, Bianca

AU - Miele, Egidio

AU - Desole, Maria S.

AU - Miele, Maddalena

AU - Serra, Pier Andrea

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AB - We showed previously that exogenous iron potentiated nitric oxide (NO) donor-induced release of striatal dopamine (DA) in freely moving rats, using microdialysis. In this study, the increase in dialysate DA induced by intrastriatal infusion of the NO-donor 3-morpholinosydnonimine (SIN-1, 1.0 mM for 180 min) was scarcely affected by Ca2+ omission. N-methyl-d-glucamine dithiocarbamate (MGD) is a thiol compound whose NO trapping activity is potentiated by iron(II). Intrastriatal co-infusion of MGD either alone or associated with iron(II), however, potentiated SIN-1-induced increases in dialysate DA. In contrast, co-infusion of the NO trapper 4-(carboxyphenyl)-4, 4,5,5-tetramethylimidazole-1-oxyl 3-oxide (carboxy-PTIO) significantly attenuated the increase in dialysate DA induced by SIN-1 (5.0 mM for 180 min). SIN-1+MGD+iron(II)-induced increases in dialysate DA were inhibited by Ca 2+ omission or co-infusion of either deferoxamine or the L-type (Cav 1.1-1.3) Ca2+ channel inhibitor nifedipine; in contrast, the increase was scarcely affected by co-infusion of the N-type (Cav 2.2) Ca2+ channel inhibitor ω-conotoxin GVIA. These results demonstrate that exogenous NO-induced release of striatal DA is independent on extracellular Ca2+; however, in presence of the NO trapper MGD, NO may preferentially react with either endogenous or exogenous iron to form a complex which releases striatal DA with an extracellular Ca 2+-dependent and nifedipine-sensitive mechanism.

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