Publications by authors named "M V Turovskaya"
Article Synopsis
- Genetic mutations during brain development are crucial in causing epilepsy, especially when related to transcription factors like Sip1, making it challenging to find effective treatments.
- Researchers used mice with a deletion of the Sip1 gene to study epilepsy and cognitive impairment, focusing on the role of brain-derived neurotrophic factor (BDNF) in neuron protection.
- Findings showed that overexpressing BDNF in Sip1 mice eliminated seizure activity and improved neuron survival, suggesting BDNF could help inhibit epilepsy and restore cognitive functions in affected individuals.
The aim of the study was to investigate the mechanisms of Ca oscillation generation upon activation of connexin-43 and regulation of the lipolysis/lipogenesis balance in white adipocytes through vesicular ATP release. With fluorescence microscopy it was revealed that a decrease in the concentration of extracellular calcium ([Ca]) results in two types of Ca responses in white adipocytes: Ca oscillations and transient Ca signals. It was found that activation of the connexin half-channels is involved in the generation of Ca oscillations, since the blockers of the connexin hemichannels-carbenoxolone, octanol, proadifen and Gap26-as well as Cx43 gene knockdown led to complete suppression of these signals.
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- Transcription factors Satb1 and Satb2 are essential for the development and maturation of neurons, influencing key receptor genes involved in neurotransmission.
- Alterations in Satb1 or Satb2 expression can disrupt neurotransmission and potentially contribute to neurodegenerative processes.
- This study reveals that deletion of either transcription factor leads to heightened NMDA receptor responses and altered calcium signaling, as well as changes in AMPA and KA receptor sensitivities, impacting neuronal maturation and GABAergic function.
Various types of cells demonstrate ubiquitous rhythmicity registered as simple and complex Ca-oscillations, spikes, waves, and triggering phenomena mediated by G-protein and tyrosine kinase coupled receptors. Phospholipase C/IP-receptors (PLC/IPR) and endothelial NO-synthase/Ryanodine receptors (NOS/RyR)-dependent Ca signaling systems, organized as multivariate positive feedback generators (PLC-G and NOS-G), underlie this rhythmicity. Loss of rhythmicity at obesity may indicate deregulation of these signaling systems.
View Article and Find Full Text PDFObjective: This study aimed to investigate the connection between the mutation of the transcription factor and impaired Ca-signaling, which reflects changes in neurotransmission in the cerebral cortex .
Methods: We used mixed neuroglial cortical cell cultures derived from mutant mice. The cells were loaded with a fluorescent ratiometric calcium-sensitive probe Fura-2 AM and epileptiform activity was modeled by excluding magnesium ions from the external media or adding a GABA(A) receptor antagonist, bicuculline.