 |
 Previous Article | Next Article 
Volume 17, Number 14,
Issue of July 15, 1997
pp. 5407-5415
Copyright ©1997 Society for Neuroscience
Absence of a Persistently Elevated 37 kDa Fos-Related Antigen and
AP-1-Like DNA-Binding Activity in the Brains of Kainic Acid-Treated
fosB Null Mice
Received March 6, 1997; revised April 23, 1997; accepted May 1, 1997.
Allan Mandelzys1,
Mary
Ann Gruda2,
Rodrigo Bravo2, and
James I. Morgan1
1 Department of Developmental Neurobiology, St. Jude
Children's Research Hospital, Memphis, Tennessee 38105, and
2 Department of Oncology, Bristol Myers-Squibb
Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000
Chronic stimulation of the nervous system or acute administration
of kainic acid results in a persistent increase in AP-1-like DNA-binding activity in the brain. However, the composition and function of these AP-1 complexes remain controversial. By comparing wild-type and fosB-null mice treated with kainic acid,
we establish that the complexes comprise JunD in association with an
~37 kDa  -FosB species. -FosB was expressed persistently in
neurons in many areas of the CNS, even though fosB mRNA
only increased transiently. This implies that the 37 kDa protein is
very stable. fosB / mice are predisposed to seizures.
Therefore, the chronic expression of -FosB elicited by kainic acid
seizures may be indicative of a compensatory/protective role in the
pathophysiology of epilepsy.
Key words:
-FosB;
JunD;
chronic Fra;
epileptogenesis;
protein
stability;
neurons
This article has been cited by other articles:
|
|
|
|
 
C. H. Liu, J. Q. Ren, J. Yang, C.-m. Liu, J. B. Mandeville, B. R. Rosen, P. G. Bhide, Y. Yanagawa, and P. K. Liu
DNA-Based MRI Probes for Specific Detection of Chronic Exposure to Amphetamine in Living Brains
J. Neurosci.,
August 26, 2009;
29(34):
10663 - 10670.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Zhu, M. Lee, S. Agatsuma, and N. Hiroi
Pleiotropic impact of constitutive fosB inactivation on nicotine-induced behavioral alterations and stress-related traits in mice
Hum. Mol. Genet.,
April 1, 2007;
16(7):
820 - 836.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. G. Ulery, G. Rudenko, and E. J. Nestler
Regulation of {Delta}FosB Stability by Phosphorylation.
J. Neurosci.,
May 10, 2006;
26(19):
5131 - 5142.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. I. Perrotti, Y. Hadeishi, P. G. Ulery, M. Barrot, L. Monteggia, R. S. Duman, and E. J. Nestler
Induction of {Delta}FosB in Reward-Related Brain Structures after Chronic Stress
J. Neurosci.,
November 24, 2004;
24(47):
10594 - 10602.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. C. Elliott and C. M. Gall
Changes in Activating Protein 1 (AP-1) Composition Correspond with the Biphasic Profile of Nerve Growth Factor mRNA Expression in Rat Hippocampus after Hilus Lesion-Induced Seizures
J. Neurosci.,
March 15, 2000;
20(6):
2142 - 2149.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. Hiroi, G. J. Marek, J. R. Brown, H. Ye, F. Saudou, V. A. Vaidya, R. S. Duman, M. E. Greenberg, and E. J. Nestler
Essential Role of the fosB Gene in Molecular, Cellular, and Behavioral Actions of Chronic Electroconvulsive Seizures
J. Neurosci.,
September 1, 1998;
18(17):
6952 - 6962.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Chen, M. B. Kelz, G. Zeng, N. Sakai, C. Steffen, P. E. Shockett, M. R. Picciotto, R. S. Duman, and E. J. Nestler
Transgenic Animals with Inducible, Targeted Gene Expression in Brain
Mol. Pharmacol.,
September 1, 1998;
54(3):
495 - 503.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
E. J. Nestler and G. K. Aghajanian
Molecular and Cellular Basis of Addiction
Science,
October 3, 1997;
278(5335):
58 - 63.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
N. Hiroi, J. R. Brown, C. N. Haile, H. Ye, M. E. Greenberg, and E. J. Nestler
FosB mutant mice: Loss of chronic cocaine induction of Fos-related proteins and heightened sensitivity to cocaine's psychomotor and rewarding effects
PNAS,
September 16, 1997;
94(19):
10397 - 10402.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
