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Information × Registration Number 0226U002232, (0124U001556) , R & D reports Title The influence of neurotransmitters on the signaling of neuronal calcium-sensing proteins in CNS neurons in normal and pathological conditions. popup.stage_title Проміжний звіт. Транслокації НКС білків та їх мутантів, що виникають при різних фізіологічно значимих патернах активності нейронів гіпокампу. Вплив нейромедіаторів в нейронах гіпокампу на концентрацію внутрішньоклітинних іонів кальцію, [Ca2+]in, кальцієвий струм та [Ca2+]in транзієнти, індуковані деполярізацією мембрани, що викликає (IsAHP) або довготривалу депресію (LTD) та на транслокації НКС. Розробка математичної моделі нейрона з компонентами гіпокальцинової сигналізації при дії нейромедіаторів. Head Bilan Pavlo V., Доктор біологічних наук Registration Date 12-02-2026 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.description2 Using advanced FRET approaches, we have revealed significant non-uniform translocations of NCS hypocalcin in response to induction of NMDA receptor-dependent long-term depression, localized along the trunk of the dendritic tree and within dendritic spines. The use of additional fluorescent labels has allowed us to identify zones of active NCS incorporation into compact regions adjacent to postsynaptic dendritic junctions. Under conditions of precise control of NMDA application, we have characterized the redistribution of hypocalcin and established the level of receptor activation at which the maximum protein incorporation into the membranes of dendritic structures occurs. We have shown that differences in the calcium sensitivity of NCS family proteins are determined not only by the interaction of such proteins with calcium ions in the cytosol, but also by their interaction with the membrane. Product Description popup.authors Volodimir V. Krotov Павло В. Білан Oleksandr V. Dovhan Volodymyr Р. Cherkas Mykola I. Kononenko Andrii V. Dromaretskyi Olena E. Saftenku Oleksii V. Gryshchenko Sheremet Yevhenii Yu. Borys O. Olifirov popup.nrat_date 2026-02-12 Close