NDLI: Hippocampal long-term potentiation is impaired in mice lacking brain-derived neurotrophic factor.

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Hippocampal long-term potentiation is impaired in mice lacking brain-derived neurotrophic factor.

Content Provider	Semantic Scholar
Author	Korte, Martin Carroll, Paul Wolf, Eckhard Brem, Gottfried Thoenen, Hans Bonhoeffer, Tobias
Copyright Year	1995
Abstract	Brain-derived neurotrophic factor (BDNF), a member of the nerve growth factor (NGF) gene family, has been shown to influence the survival and differentiation of specific classes of neurons in vitro and in vivo. The possibility that neurotrophins are also involved in processes of neuronal plasticity has only recently begun to receive attention. To determine whether BDNF has a function in processes such as long-term potentiation (LTP), we produced a strain of mice with a deletion in the coding sequence of the BDNF gene. We then used hippocampal slices from these mice to investigate whether LTP was affected by this mutation. Homo- and heterozygous mutant mice showed significantly reduced LTP in the CA1 region of the hippocampus. The magnitude of the potentiation, as well as the percentage of cases in which LTP could be induced successfully, was clearly affected. According to the criteria tested, important pharmacological, anatomical, and morphological parameters in the hippocampus of these animals appear to be normal. These results suggest that BDNF might have a functional role in the expression of LTP in the hippocampus.
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://www.pnas.org/content/92/19/8856.full.pdf
PubMed reference number	7568031v1
Volume Number	92
Issue Number	19
Journal	Proceedings of the National Academy of Sciences of the United States of America
Language	English
Access Restriction	Open
Subject Keyword	BDNF gene Brain-Derived Neurotrophic Factor CA1 field Class Deletion Mutation Growth Factor Long-Term Potentiation NGF gene Nerve Growth Factors Neuronal Plasticity Open Reading Frames Pharmacology chemosensitization/potentiation
Content Type	Text
Resource Type	Article

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