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Long-term induction of fos-related antigen-2 after methamphetamine-, methylenedioxymethamphetamine-, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- and trimethyltin-induced brain injury.

Authors
Pennypacker-KR; Yang-X; Gordon-MN; Benkovic-S; Miller-D; O'Callaghan-JP
Source
Neuroscience 2000 Nov; 101(4):913-919
NIOSHTIC No.
20020778
Abstract
A long-term induction of Fos-related antigens has been shown in neurons after brain injury, suggesting that Fos-related antigens are involved in enhancing the transcription of genes related to the process of regeneration and repair. In the present study, we report that levels of Fos-related antigen-2 are elevated in several models of chemically induced brain injury. Trimethyltin, which causes degeneration of neurons primarily in the hippocampus and other limbic regions, results in a five-fold induction of Fos-related antigen-2 immunoreactivity in neurons in the pyramidal and dentate layers of the hippocampus starting at seven days post-treatment and persisting for 60days. Methamphetamine and methylenedioxymethamphetamine, agents which cause degeneration of dopaminergic nerve terminals in the striatum of the mouse, cause an increase in Fos-related antigen-2 immunoreactivity which begins at three days post-treatment and returns to basal levels by days 5 and 15, respectively. Treatment with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine elevated levels of Fos-related antigen-2 in the mouse striatum at three days post-treatment. This abbreviated time-course of Fos-related antigen-2 induction is consistent with less severe insult (terminal damage) relative to trimethyltin (cell death), but induction occurs during the period of regeneration and repair in both models. Dexfenfluramine, a non-neurotoxic amphetamine, does not induce Fos-related antigen-2 expression. Decreasing core temperature of the mouse, which blocks amphetamine-induced neurotoxicity, also blocks Fos-related antigen-2 induction.In summary, Fos-related antigen-2 is induced in models of both cell death and terminal degeneration, suggesting that this transcription factor may serve as a universal signal transduction molecule involved in the regulation of genes related to regeneration and repair in the CNS.
Keywords
Antigens; Brain-damage; Brain-disorders; Injuries; Traumatic-injuries; Neurotoxicity; Neurotoxic-effects; Neurotoxicology; Models; Laboratory-animals; Animals; Animal-studies; Central-nervous-system; Central-nervous-system-disorders
CODEN
NRSCDN
CAS No.
1631-73-8
Publication Date
20001130
Document Type
Journal Article
Email Address
kpennypa@hsc.usf.edu
Fiscal Year
2001
NTIS Accession No.
NTIS Price
Issue of Publication
4
ISSN
0306-4522
NIOSH Division
HELD
Source Name
Neuroscience
State
WV; FL
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