Bdnf, short for Brain-derived neurotrophic factor, is one of the most widely distributed and studied neurotrophins in the mammalian brain. It signals through the tropomycin receptor kinase B (TrkB) and the low-affinity p75 neurotrophin receptor (p75NTR). Bdnf plays a crucial role in the growth, development, and plasticity of glutamatergic and GABAergic synapses, and influences serotonergic and dopaminergic neurotransmission via modulation of neuronal differentiation. It is also important for the transformation of synaptic activity into long-term memories and for adult neurogenesis in the hippocampus [1].

In antidepressant research, genetic manipulations disrupting BDNF signaling in mice attenuated the antidepressant-like response to conventional antidepressants. BDNF and TrkB conditional knockout mice showed abolished antidepressant-like response to ketamine, highlighting BDNF as an essential determinant of antidepressant efficacy [2]. In Parkinson's disease, although direct delivery of exogenous BDNF or gene therapy to enhance its expression did not relieve symptoms, physical training-induced BDNF increase was neuroprotective in animal models, suggesting a potential adjunctive therapy role [3].

In conclusion, Bdnf is vital for normal neuronal development, synaptic plasticity, and neurotransmission. Gene knockout and conditional knockout mouse models have revealed its significance in diseases like depression and Parkinson's disease. These models help us understand the role of Bdnf in specific biological processes and offer potential therapeutic directions for related diseases.