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Information × Registration Number 0124U001556, ( 0225U003234  0226U002232  ) R & D request Title The influence of neurotransmitters on the signaling of neuronal calcium-sensing proteins in CNS neurons in normal and pathological conditions. Head Bilan Pavlo V., Доктор біологічних наук Registration Date 09-02-2024 Organization Bogomolets Institute of Physiology of the National Academy of Sciences of Ukraine popup.description1 The goal of the stated scientific development is to study the influence of neurotransmitters, primarily acetylcholine and adrenaline, on the functioning of neuronal calcium sensor (NCS) proteins in CNS neurons in normal and pathological conditions. If we use general images, then we can say that any fairly complex signal system (you can use the terms "encoding/decoding") in the body receives information from the outside, processes it and sends the result in an adequate form to the appropriate targets. Normally, there is a delicate balance between these processes, but with pathology, it is disturbed, and then there is a dysfunction of the entire system. As such a signaling system, we have over the past decades studied the signaling of neuronal calcium-sensing proteins in CNS neurons, namely the functioning of Ca2+-dependent hypocalcin (HPSA) in hippocampal neurons, and recently showed at the molecular level how point mutations in a specific gene that encodes NSAIDs can cause phenomena that are characteristic of symptoms of primary dystonia (DYT2). It is also known that some neurotransmitters that play a significant role in the functioning of the central nervous system, for example, acetylcholine and adrenaline, can affect the level of intracellular concentration of Ca2+ or the lipid composition of membranes and thereby can affect the Ca2+-dependent incorporation of NKS proteins into membranes and their signaling. However, such regulation for NKS proteins is unexplored. We plan to investigate these phenomena at the molecular and cellular levels for both wild-type NKS proteins and their mutant forms, in particular those responsible for DYT2. popup.nrat_date 2024-12-09 Close