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. Recent studies suggest that neurotrophins, including BDNF, may also be involved in neuronal plasticity. To investigate whether BDNF plays a role in long-term potentiation (LTP), a key process in synaptic plasticity, researchers created a strain of mice with a deletion in the BDNF gene. They found that both homozygous and heterozygous mutant mice showed significantly reduced LTP in the hippocampus. The magnitude of LTP and the percentage of successful inductions were affected. Despite these impairments, important pharmacological, anatomical, and morphological parameters in the hippocampus appeared normal. These results suggest that BDNF may have a functional role in the expression of LTP in the hippocampus. The study used gene-targeting techniques to create BDNF-deficient mice. These mice showed impaired LTP, with homozygous mutants showing age-dependent changes. Heterozygous mutants also showed reduced LTP, though to a lesser extent. Control experiments indicated that the failure to induce LTP was not due to impaired synaptic transmission. Pharmacological tests showed that LTP in BDNF-deficient mice was blocked by NMDA antagonists, indicating it was pharmacologically normal. However, when LTP could not be induced, it was not due to a lack of NMDA responses. The study also showed that BDNF is not the only factor involved in LTP. In some cases, LTP could still be induced without BDNF. This suggests that while BDNF plays a critical role in LTP, it is not essential under all circumstances. The results indicate that BDNF has a functional role in the expression of LTP in the hippocampus. The study also found that BDNF-deficient mice showed no obvious anatomical or morphological abnormalities, suggesting that the impairment in LTP is due to a functional role of BDNF in synaptic plasticity.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. Recent studies suggest that neurotrophins, including BDNF, may also be involved in neuronal plasticity. To investigate whether BDNF plays a role in long-term potentiation (LTP), a key process in synaptic plasticity, researchers created a strain of mice with a deletion in the BDNF gene. They found that both homozygous and heterozygous mutant mice showed significantly reduced LTP in the hippocampus. The magnitude of LTP and the percentage of successful inductions were affected. Despite these impairments, important pharmacological, anatomical, and morphological parameters in the hippocampus appeared normal. These results suggest that BDNF may have a functional role in the expression of LTP in the hippocampus. The study used gene-targeting techniques to create BDNF-deficient mice. These mice showed impaired LTP, with homozygous mutants showing age-dependent changes. Heterozygous mutants also showed reduced LTP, though to a lesser extent. Control experiments indicated that the failure to induce LTP was not due to impaired synaptic transmission. Pharmacological tests showed that LTP in BDNF-deficient mice was blocked by NMDA antagonists, indicating it was pharmacologically normal. However, when LTP could not be induced, it was not due to a lack of NMDA responses. The study also showed that BDNF is not the only factor involved in LTP. In some cases, LTP could still be induced without BDNF. This suggests that while BDNF plays a critical role in LTP, it is not essential under all circumstances. The results indicate that BDNF has a functional role in the expression of LTP in the hippocampus. The study also found that BDNF-deficient mice showed no obvious anatomical or morphological abnormalities, suggesting that the impairment in LTP is due to a functional role of BDNF in synaptic plasticity.