PMID- 15049510
OWN - NLM
STAT- MEDLINE
DCOM- 20040628
LR  - 20191026
IS  - 0272-4340 (Print)
IS  - 0272-4340 (Linking)
VI  - 24
IP  - 1
DP  - 2004 Feb
TI  - Endogenous dopamine maintains synchronous oscillation of intracellular calcium in 
      primary cultured-mouse midbrain neurons.
PG  - 51-61
AB  - We demonstrated synchronous oscillation of intracellular Ca2+ in cultured-mouse 
      mid-brain neurons. This synchronous oscillation was thought to result from 
      spontaneous and synchronous neural bursts in a synaptic neural network. We also 
      examined the role of endogenous dopamine in neural networks showing synchronous 
      oscillation. Immunocytochemical study revealed a few tyrosine hydroxylase 
      (TH)-positive dopaminergic neurons, and that cultured neurons expressed 
      synaptophysin and synapsin I. Western blot analyses comfirmed synaptophysin, TH, 
      and 2 types of dopamine receptor (DR), D1R and D2R expression. The synchronous 
      oscillation in midbrain neurons was abolished by the application of 
      R(-)-2-amino-5-phosphonopentanoic acid (AP-5) as an N-methyl-D-aspartate receptor 
      (NMDAR) antagonist. This result suggests that the synchronous oscillation in 
      midbrain neurons requires glutamatergic transmissions, as was the case in 
      previously reported cortical neurons. SCH-12679, a D1R antagonist, inhibited 
      synchronous oscillation in midbrain neurons, while raclopride, a D2R antagonist, 
      induced a transient increase of intracellular Ca2+ and inhibited synchronous 
      oscillation. We consider that endogenous dopamine maintains synchronous 
      oscillation of intracellular Ca2+ through D1R and D2R, and that these DRs 
      regulate intracellular Ca2+in distinctly different ways. Synchronous oscillation 
      of midbrain neurons would be a useful tool for in vitro researches into various 
      neural disorders directly or indirectly caused by dopaminergic neurons.
FAU - Yasumoto, Fumie
AU  - Yasumoto F
AD  - Department of Biomedical Science, Graduate School of Agricultural and Life 
      Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan. 
      aa37169@mail.eccu-tokyo.ac.jp
FAU - Negishi, Takayuki
AU  - Negishi T
FAU - Ishii, Yoshiyuki
AU  - Ishii Y
FAU - Kyuwa, Shigeru
AU  - Kyuwa S
FAU - Kuroda, Yoichiro
AU  - Kuroda Y
FAU - Yoshikawa, Yasuhiro
AU  - Yoshikawa Y
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Cell Mol Neurobiol
JT  - Cellular and molecular neurobiology
JID - 8200709
RN  - 0 (Dopamine Antagonists)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Receptors, Dopamine D1)
RN  - 0 (Receptors, Dopamine D2)
RN  - 0 (Synaptophysin)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - SY7Q814VUP (Calcium)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Action Potentials/drug effects/physiology
MH  - Animals
MH  - Biological Clocks/drug effects/*physiology
MH  - Calcium/*metabolism
MH  - Calcium Signaling/drug effects/*physiology
MH  - Cells, Cultured
MH  - Dopamine/*metabolism
MH  - Dopamine Antagonists/pharmacology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Fetus
MH  - Intracellular Fluid/drug effects/metabolism
MH  - Mesencephalon/cytology/drug effects/*metabolism
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Neurons/cytology/drug effects/*metabolism
MH  - Receptors, Dopamine D1/drug effects/metabolism
MH  - Receptors, Dopamine D2/drug effects/metabolism
MH  - Synaptic Transmission/drug effects/physiology
MH  - Synaptophysin/metabolism
MH  - Tyrosine 3-Monooxygenase/metabolism
EDAT- 2004/03/31 05:00
MHDA- 2004/06/29 05:00
CRDT- 2004/03/31 05:00
PHST- 2004/03/31 05:00 [pubmed]
PHST- 2004/06/29 05:00 [medline]
PHST- 2004/03/31 05:00 [entrez]
AID - 10.1023/b:cemn.0000012724.79184.b6 [doi]
PST - ppublish
SO  - Cell Mol Neurobiol. 2004 Feb;24(1):51-61. doi: 
      10.1023/b:cemn.0000012724.79184.b6.