Brain-derived neurotrophic factor (BDNF), encoded by the BDNF gene located on chromosome 11p14.1 in humans, is one of the most extensively studied and important neurotrophic factors in the mammalian central and peripheral nervous systems. It plays an integral role in neural development, maintenance, and plasticity. BDNF is synthesized as a precursor protein (proBDNF), which is proteolytically hydrolyzed to obtain the mature, biologically active form. Mature BDNF acts primarily by binding to its high-affinity receptor, tropomyosin receptor kinase B (TrkB), thereby triggering intracellular signaling cascades (including MAPK, PI3K/Akt, and PLCγ pathways) that promote neuronal survival, differentiation, and the growth and guidance of axons and dendrites. Crucially, BDNF is a key mediator of synaptic plasticity, the cellular basis of learning and memory. It enhances synaptic transmission, promotes long-term potentiation (LTP), and influences neurogenesis in the adult hippocampus. Thus, dysregulation of BDNF expression, processing, or signaling is strongly associated with a variety of neurological and psychiatric disorders, including depression, anxiety, Alzheimer''s disease, Parkinson''s disease, Huntington''s disease, epilepsy, and chronic pain syndromes.
Human BDNF Adenoviral Particles are a powerful and widely used recombinant viral vector technology designed to efficiently deliver and express the human BDNF gene into a variety of mammalian cell types, both in vitro and in vivo. These particles are based on modified human adenoviruses, typically serotype 5 (Ad5), that have been engineered to render them replication incompetent. Adenoviral vectors offer significant advantages: they can infect both dividing and non-dividing cells (critical for neurons), achieve very high transduction efficiencies in a variety of cell types (including neurons, glial cells, muscle cells), allow for rapid onset of transgene expression, and can accommodate relatively large transgene inserts. Human BDNF Adenoviral Particles are an indispensable tool in neuroscience research, enabling researchers to study the role of BDNF in specific cell populations or brain regions, rescue BDNF deficiencies in disease models, explore signaling pathways, and evaluate potential therapeutic benefits in preclinical studies of neurological disorders.
Studies have found that berberine can inhibit the progression of depression, but its specific mechanism is still unclear. microRNA (miRNA) is believed to play an important role in the progression of depression. However, whether berberine is involved in regulating the progression of depression through miRNA is still unclear. Here, the study showed that berberine can inhibit the depressive behavior of CUMS mice and promote the growth of hippocampal neurons by targeting miR-34b-5p and miR-470-5p. In addition, the researchers found that BDNF is a target of miR-34b-5p and miR-470-5p. Overexpressed BDNF can reverse the regulation of miR-34b-5p and miR-470-5p on depressive behavior and hippocampal neuron growth in CUMS mice. In addition, berberine can promote the expression of BDNF, thereby regulating the depressive behavior and hippocampal neuron growth in CUMS mice. These findings suggest that berberine may inhibit the progression of depression by regulating the miR-34b-5p/miR-470-5p/BDNF axis.
To evaluate whether miR-34b-5p regulates depressive behavior and hippocampal neuron growth in CUMS mice by targeting BDNF, the researchers simultaneously injected miR-34b-5p overexpression adenovirus and BDNF overexpression adenovirus into mice. Overexpressed BDNF can effectively restore the inhibitory effect of miR-34b-5p mimics on BDNF expression in the hippocampus of CUMS mice (Figure 1A). By examining the depressive behavior of CUMS mice, the researchers found that overexpression of BDNF significantly reversed the effects of miR-34b-5p on the reduction of sucrose preference and swimming time and the increase of immobility time in CUMS mice (Figure 1B-D). In addition, overexpressed BDNF eliminated the inhibitory effects of miR-34b-5p on hippocampal neuron viability and the promotion of apoptosis and TUNEL-positive cells (Figure 1E-H).
Figure 1. MiR-34b-5p and BDNF regulated CUMS mice depressive behavior and hippocampal neurons growth. (Zhan Y, et al., 2021)
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The Human BDNF adenoviral particles exceeded expectations—high transduction efficiency and measurable functional effects in our neuronal cultures. Perfect for studying neurotrophic pathways!
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