 |
 Previous Article | Next Article 
The Journal of Neuroscience, May 1, 1999, 19(9):3345-3352
Tonic Dopamine Inhibition of L-Type Ca2+ Channel
Activity Reduces  1D Ca2+ Channel Gene
Expression
Daniel M.
Fass1,
Koichi
Takimoto2,
Richard E.
Mains3, and
Edwin S.
Levitan2
1 Department of Neuroscience, University of Pittsburgh,
Pittsburgh, Pennsylvania 15260, 2 Department of
Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh,
Pennsylvania 15261, and 3 Neuroscience Department, Johns
Hopkins University School of Medicine, Baltimore, Maryland 21205
Hormones and neurotransmitters have both short-term and long-term
modulatory effects on the activity of voltage-gated
Ca2+ channels. Although much is known about the
signal transduction underlying short-term modulation, there is far less
information on mechanisms that produce long-term effects. Here, the
molecular basis of long-lasting suppression of Ca2+
channel current in pituitary melanotropes by chronic dopamine exposure
is examined. Experiments involving in vivo and in
vitro treatments with the dopaminergic drugs haloperidol,
bromocriptine, and quinpirole show that D2 receptors persistently
decrease  1D L-type Ca2+ channel mRNA
and L-type Ca2+ channel current without altering
channel gating properties. In contrast, another L-channel
(1C) mRNA and P/Q-channel
(1A) mRNA are unaffected. The downregulation of
1D mRNA does not require decreases in cAMP levels or
P/Q-channel activity. However, it is mimicked and occluded by
inhibition of L-type channels. Thus, interruption of the positive
feedback between L-type Ca2+ channel activity and
1D gene expression can account for the long-lasting
regulation of L-current produced by chronic activation of D2 dopamine receptors.
Key words:
L-type Ca2+ channel; dopamine; D2
receptor; melanotrope; nimodipine; haloperidol; quinpirole
Copyright © 1999 Society for Neuroscience 0270-6474/99/1993345-08$05.00/0
This article has been cited by other articles:
|
|
|
|
 
I. Dudanova, S. Sedej, M. Ahmad, H. Masius, V. Sargsyan, W. Zhang, D. Riedel, F. Angenstein, D. Schild, M. Rupnik, et al.
Important Contribution of {alpha}-Neurexins to Ca2+-Triggered Exocytosis of Secretory Granules
J. Neurosci.,
October 11, 2006;
26(41):
10599 - 10613.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Sedej, T. Tsujimoto, R. Zorec, and M. Rupnik
Voltage-activated Ca2+ channels and their role in the endocrine function of the pituitary gland in newborn and adult mice
J. Physiol.,
March 15, 2004;
555(3):
769 - 782.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Jurkat-Rott and F. Lehmann-Horn
The impact of splice isoforms on voltage-gated calcium channel {alpha}1 subunits
J. Physiol.,
February 1, 2004;
554(3):
609 - 619.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. D. Kline, K. N. Takacs, E. Ficker, and D. L. Kunze
Dopamine Modulates Synaptic Transmission in the Nucleus of the Solitary Tract
J Neurophysiol,
November 1, 2002;
88(5):
2736 - 2744.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
X.-F. Zhang, D. C. Cooper, and F. J. White
Repeated Cocaine Treatment Decreases Whole-Cell Calcium Current in Rat Nucleus Accumbens Neurons
J. Pharmacol. Exp. Ther.,
June 1, 2002;
301(3):
1119 - 1125.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. Carabelli, J. M Hernandez-Guijo, P. Baldelli, and E. Carbone
Direct autocrine inhibition and cAMP-dependent potentiation of single L-type Ca2+ channels in bovine chromaffin cells
J. Physiol.,
April 1, 2001;
532(1):
73 - 90.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. D. Brewer, V. Thibault, K.-C. Chen, M. C. Langub, P. W. Landfield, and N. M. Porter
Vitamin D Hormone Confers Neuroprotection in Parallel with Downregulation of L-Type Calcium Channel Expression in Hippocampal Neurons
J. Neurosci.,
January 1, 2001;
21(1):
98 - 108.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
