Elucidating the calcium control of maxi-K potassium channels in neurodevelopmental disorders
This project investigates how changes in specific brain cell proteins, which control calcium signalling, affect brain development and function.
By studying these changes, we aim to understand how they contribute to severe developmental brain disorders.
Pathogenic mutations in voltage-gated calcium (Cav) and sodium (Nav) channels can lead to severe infantile encephalopathy. Dysregulated calcium influx through these mutated Cav and Nav channels can alter the modulation of calcium-activated maxi-K channels, contributing to disrupted neuronal excitability and synaptic transmission.
Methods used in this research include patch-clamp electrophysiology, high-speed calcium imaging and mouse models of genetic epilepsy.
Aim
- To elucidate the functional crosstalk between maxi-K channels and pathogenic Cav or Nav variants in heterologous expression systems and in real or virtual neurons.
- Enhance the understanding of the molecular pathophysiology impacting excitability, synaptic function, and calcium homeostasis.
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