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

TLDR

BDNF, a neurotrophin, is known to influence neuronal survival and differentiation, and recent evidence indicates neurotrophins also participate in neuronal plasticity. The study aimed to determine whether BDNF is required for long‑term potentiation by generating mice lacking the BDNF coding sequence. Hippocampal slices from these BDNF‑deficient mice were used to assess LTP induction and magnitude. Deletion of BDNF markedly reduced CA1 LTP magnitude and induction frequency, while other hippocampal parameters remained normal, underscoring BDNF’s essential role in LTP expression.

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.