Publications by authors named "D Vasylyev"
Voltage-gated sodium channels (VGSCs) are best known for their role in the generation and propagation of action potentials in neurons, muscle cells, and cardiac myocytes, which have traditionally been labeled as 'excitable'. However, emerging evidence challenges this traditional perspective. It is now clear that VGSCs are also expressed in a broad spectrum of cells outside the neuromuscular realm, where they regulate diverse cellular functions.
View Article and Find Full Text PDFArticle Synopsis
- This study investigates how voltage-gated sodium channels Nav1.7 and Nav1.8 work together in dorsal root ganglion (DRG) neurons, particularly focusing on the impact of a mutation in Nav1.7 associated with neuropathic pain known as inherited erythromelalgia (IEM).
- Researchers found that Nav1.8 significantly increases the likelihood of action potential (AP) generation near the voltage threshold, outperforming Nav1.7 in terms of channel open-probability at -21.9 mV by nine times.
- Reducing Nav1.8 current by 25-50% can decrease the excitability of DRG neurons with the Nav1.7
Ion channels in osteoarthritis: emerging roles and potential targets.
Nat Rev Rheumatol
September 2024
Article Synopsis
- * Research highlights the role of ion channels in OA development, suggesting they could be key targets for new treatments aimed at modifying disease progression and alleviating symptoms.
- * The review covers various types of ion channels involved in OA and discusses ongoing research, potential drug development, and the importance of ion channel biology in improving OA treatment strategies.
Article Synopsis
- * Researchers identified Na1.7 as a VGSC associated with OA, revealing its presence in human OA chondrocytes and its role in regulating OA's progression and pain perception.
- * Blocking Na1.7 pharmacologically not only slows down structural damage in joints but also alleviates pain, highlighting its potential as a target for non-opioid pain relief and disease modification in OA patients.
We show here that hyperpolarization-activated current (I ) unexpectedly acts to inhibit the activity of dorsal root ganglion (DRG) neurons expressing WT Nav1.7, the largest inward current and primary driver of DRG neuronal firing, and hyperexcitable DRG neurons expressing a gain-of-function Nav1.7 mutation that causes inherited erythromelalgia (IEM), a human genetic model of neuropathic pain.
View Article and Find Full Text PDF