Dopamine induces apoptosis in young, but not in neonatal, neurons via Ca2+-dependent signal.

Dopamine induces apoptosis in young, but not in neonatal, neurons via Ca2+-dependent signal. Research Abstract Details 

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Dopamine induces apoptosis in young, but not in neonatal, neurons via Ca2+-dependent signal. Abstract Text:

Kousaku Iwatsubo,Sayaka Suzuki,Chanxia Li,Takashi Tsunematsu,Fumi Nakamura,Satoshi Okumura,Motohiko Sato,Susumu Minamisawa,Yoshiyuki Toya,Satoshi Umemura,Yoshihiro Ishikawa,Kousaku Iwatsubo,Sayaka Suzuki,Chanxia Li,Takashi Tsunematsu,Fumi Nakamura,Satoshi Okumura,Motohiko Sato,Susumu Minamisawa,Yoshiyuki Toya,Satoshi Umemura,Yoshihiro Ishikawa,

Dopamine signaling plays a major role in regulation of neuronal apoptosis. During the postnatal period, dopamine signaling is known to be dramatically changed in the striatum. However, because it is difficult to culture neurons after birth, little is known about developmental changes in dopamine-mediated apoptosis. To examine such changes, we established the method of primary culture of striatal neurons from 2- to 3-wk-old (young) mice. Dopamine, via D(1)-like receptors, induced apoptosis in young, but not neonatal, striatal neurons, suggesting that the effect of dopamine on apoptosis changed with development. In contrast, although isoproterenol (Iso), a beta-adrenergic receptor agonist, increased cAMP production to a greater degree than dopamine, Iso did not increase apoptosis in striatal neurons from young and neonatal mice, suggesting a minor role of cAMP in dopamine-mediated apoptosis. Next, we examined the effect of dopamine on Ca(2+) signaling. Dopamine, but not Iso, markedly increased intracellular Ca(2+) in striatal neurons from young mice, and Ca(2+)-chelating agents abolished dopamine-induced apoptosis, suggesting that Ca(2+) played a major role in the dopamine-mediated apoptosis pathway. In contrast, dopamine failed to increase intracellular Ca(2+) in neonatal neurons, and the expression of PLC, which can increase intracellular Ca(2+) via D(1)-like receptor activation, was significantly greater in young than in neonatal striatal neurons. These data suggest that the developmental change in dopamine-mediated Ca(2+) signaling was responsible for differences between young and neonatal striatum in induction of apoptosis. Furthermore, the culture of young striatal neurons is feasible and may provide a new tool for developmental studies.

Dopamine induces apoptosis in young, but not in neonatal, neurons via Ca2+-dependent signal. Publishing Authors By Initials

K Iwatsubo,S Suzuki,C Li,T Tsunematsu,F Nakamura,S Okumura,M Sato,S Minamisawa,Y Toya,S Umemura,Y Ishikawa,K Iwatsubo,S Suzuki,C Li,T Tsunematsu,F Nakamura,S Okumura,M Sato,S Minamisawa,Y Toya,S Umemura,Y Ishikawa,

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Dopamine induces apoptosis in young, but not in neonatal, neurons via Ca2+-dependent signal. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: American journal of physiology. Cell physiology

VOLUME: 293

Page Numbers: C1498-508

Journal Abbreviation: Am. J. Physiol., Cell Physiol.

ISSN: 0363-6143

DAY: 5

MONTH: 09

YEAR: 2007

Dopamine induces apoptosis in young, but not in neonatal, neurons via Ca2+-dependent signal. Information

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LANGUAGE: eng

NlmUniqueID: 100901225

Dopamine induces apoptosis in young, but not in neonatal, neurons via Ca2+-dependent signal. Keywords Mesh Terms:

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Grant and Affiliation Information for Dopamine induces apoptosis in young, but not in neonatal, neurons via Ca2+-dependent signal.

AFFILIATION: Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, New Jersey Medical School-University of Medicine and Dentistry of New Jersey, Newark, New Jersey, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL-059139

ACRONYM: HL

MEDLINETA: Am J Physiol Cell Physiol

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