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PMID: 10501474 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Brain-derived neurotrophic factor transgenic mice exhibit passive avoidance deficits, increased seizure severity and in vitro hyperexcitability in the hippocampus and entorhinal cortex.

Neuroscience ·Vol. 93 ·No. 4 ·1999-00-00 ·Pages 1491-506

Croll SD, Suri C, Compton DL, Simmons MV, Yancopoulos GD, Lindsay RM, Wiegand SJ, Rudge JS, Scharfman HE

Abstract

Transgenic mice overexpressing brain-derived neurotrophic factor from the beta-actin promoter were tested for behavioral, gross anatomical and physiological abnormalities. Brain-derived neurotrophic factor messenger RNA overexpression was widespread throughout brain. Overexpression declined with age, such that levels of overexpression decreased sharply by nine months. Brain-derived neurotrophic factor transgenic mice had no gross deformities or behavioral abnormalities. However, they showed a significant passive avoidance deficit. This deficit was dependent on continued overexpression, and resolved with age as brain-derived neurotrophic factor transcripts decreased. In addition, the brain-derived neurotrophic factor transgenic mice showed increased seizure severity in response to kainic acid. Hippocampal slices from brain-derived neurotrophic factor transgenic mice showed hyperexcitability in area CA3 and entorhinal cortex, but not in dentate gyrus. Finally, area CA1 long-term potentiation was disrupted, indicating abnormal plasticity. Our data suggest that overexpression of brain-derived neurotrophic factor in the brain can interfere with normal brain function by causing learning impairments and increased excitability. The results also support the hypothesis that excess brain-derived neurotrophic factor could be pro-convulsant in the limbic system.

MeSH Terms
Age Factors Animals Avoidance Learning/physiology Behavior, Animal/physiology Blotting, Northern Brain Chemistry/genetics Brain-Derived Neurotrophic Factor/genetics Dentate Gyrus/physiopathology Electrophysiology Entorhinal Cortex/physiopathology Epilepsy/chemically induced,physiopathology Excitatory Amino Acid Agonists Gene Expression/physiology Hot Temperature In Situ Hybridization Kainic Acid Long-Term Potentiation/physiology Maze Learning/physiology Memory/physiology Mice Mice, Inbred C57BL Mice, Inbred CBA Mice, Transgenic Neuronal Plasticity/physiology Organ Culture Techniques Pain Threshold RNA, Messenger/analysis Swimming Transgenes
Chemicals
Brain-Derived Neurotrophic Factor Excitatory Amino Acid Agonists RNA, Messenger Kainic Acid
Authors & Affiliations
9 authors, click to expand affiliations / ORCID
Croll S D
Regeneron Pharmaceuticals, Tarrytown, NY 10591, USA.
Suri C
Compton D L
Simmons M V
Yancopoulos G D
Lindsay R M
Wiegand S J
Rudge J S
Scharfman H E
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Article Info
Journal
Neuroscience
Abbr.
Neuroscience
ISSN
0306-4522
DOI
10.1016/s0306-4522(99)00296-1
Published
1999-00-00
Pages
1491-506
Language
English
Region
United States
NLM ID
7605074
PMCID
PMC2504500
Subset
IM
Grants
NINDS NIH HHS · R01 NS037562 · United States
NINDS NIH HHS · R01 NS037562-02 · United States
NINDS NIH HHS · R56 NS037562 · United States
NINDS NIH HHS · NS 37562 · United States
External Links
PubMed source DOI: 10.1016/s0306-4522(99)00296-1 PMC Full Text View journal details
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