BDNF antibodies and synaptic plasticity research

Brain-derived neurotrophic factor (BDNF) is a neurotrophin which plays an important role in neuronal differentiation, migration and survival during development. Recent BDNF antibody studies have shown activity-regulated BDNF expression to be important at the synapse between neurons, affecting synaptic plasticity – the way in which synapses alter in strength in response to transmission signaling changes. We have a large neuroscience antibody catalog containing most of the antibodies used in neurological research today.

Activity-dependent expression changes occur after synaptic transmission, resulting with influx of calcium (Ca2+) which induces transcription factors to bind CaREs (calcium-response elements) in the nucleus. In 1998, Xu Tao et al showed that Ca2+-dependent BDNF regulation was mediated by the CREB (cAMP response element-binding) transmission factor, in combination with other transmission factors.

Improvements in antibody research have helped clarify the importance of activity-regulated BDNF expression in neuronal function and brain development. However, its role in synaptic plasticity has been harder to prove. In 2008 Hong et al addressed this with a series of BDNF antibody studies using mouse models demonstrating a variety of knock-in mutations. One study demonstrated specific blocking of CaRE3/CRE (the CaRE regulating Bdnf mRNA expression via CREB) in CREmKI mice.The CREmKI mutation demonstrates a subtle alteration to the nucleotide sequence, causing significant impairment of activity-dependent expression of BDNF. BDNF-deficient mice were also used, but proved nonviable.

The CREmKI mice were indistinguishable from their wild-type (normal) littermates in appearance and behavior. However, BDNF antibody assays showed activity-induced Bdnf mRNA expression to be reduced by more than 50% in cultures of embryonic neurons, and in the adult visual cortex in vivo. Decreased inhibitory synapse density was observed in both cases. A further study by K. Sakata et al in 2009 showed that disruption of promoter IV-induced Bdnf expression resulted in impairment of prefrontal cortex synaptic signaling. Taken together, these antibody studies show BDNF has a role in homeostatic plasticity, regulating the balance between excitatory and inhibitory synaptic signaling.

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