Scientists from The Francis Crick Institute and UCL Queen Square Institute of Neurology have made groundbreaking strides in understanding epilepsy's genetic complexities, specifically focusing on CDKL5 deficiency disorder (CDD). Their innovative work, recently published on bioRxiv, leverages state-of-the-art digital cage technology, providing vital insights into the role of the voltage-gated Ca2+ channel Cav2.3 in neuronal excitability.
The research team employed phosphoproteomic screening to identify Cav2.3 as a novel target of the brain-enriched kinase CDKL5. Through the use of digital cage technology, they were able to accurately monitor and record the effects of Cav2.3 phosphorylation loss on mice, revealing that it leads to slower channel inactivation, enhanced cholinergic stimulation, and increased neuronal excitability.
The study underpins the importance of digital cage technology as a key tool in neurological research, enabling non-invasive monitoring and recording of results in real-time. Digital cages provide an ideal environment for studying changes in neuronal activity and behavior, helping to elucidate the underlying mechanisms of complex disorders such as CDD.
The research also highlights the potential for Cav2.3 inhibitors in the treatment of disorders like CDD and DEE69, further demonstrating the critical role of DVC® in facilitating cutting-edge neurological research and drug discovery.
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