Department of Neuroscience, KU
Trine L. Toft-Bertelsen (MacAulay group): TRPV4 – the bridge over troubled (brain) water
Abstract: Dysregulated cerebrospinal fluid (CSF) production brings about water accumulation inside the brain and a raise in the intracranial pressure with morphological changes. Till this day the upstream regulatory mechanisms that influence such water production still are still to be defined. In recent times, a water-translocating cotransporter, NKCC1, was identified as a main contributor to CSF formation. Here, I present the regulatory role of a Ca2+ permeable ion channel, TRPV4, in CSF secretion and regulation thereof, and the coupling between TRPV4 activation and NKCC1-mediated CSF secretion.
Anna Kadkova (Balslev Sørensen group): Human disease mutations in SNAP-25 abolish binding to synaptotagmin-1
Abstract: Release of neurotransmitters is executed with microsecond precision by the assembly of the SNARE-complex between the membranes, triggered by Ca2+-binding to synaptotagmin-1. De novo mutations in the SNAREs cause severe neurodevelopmental disease, involving hyperexcitability/epilepsy and intellectual disability. However, it remains unknown which of the functions of the SNARE-complex are disrupted by disease-causing mutations. We show that the SNAP-25 mutations V48F and D166Y strongly increased the spontaneous release and reduced both the evoked release and the size of the readily releasable pool of vesicles, indicating a disturbance in the interaction between the mutated SNARE complex and synaptotagmin-1.