Research-focused article examining how age-related neuromuscular junction decline is studied and a pharmacological strategy explored to boost postsynaptic excitability.
Key Takeaways
- Aged humans and rodents show NMJ transmission failure that correlates with muscle weakness severity
- Localized loss of the skeletal muscle sodium channel NaV1.4 at the postsynaptic NMJ was identified across species
- Small molecule inhibition of the ClC-1 chloride channel improved muscle contractile and motor function in aged rats