It is generally thought that muscle excitability is controlled by only a few types of ion channels. We propose this understanding is incomplete and misses important ion channel types that regulate excitability during repetitive firing, but do not participate in a major way in firing of single action potentials. Since these currents are small, they are hard to identify and have been missed. In this proposal we will test the hypothesis that a novel current we discovered in muscle during studies of myotonia congenita and hyperkalemic periodic paralysis also plays a central role in triggering attacks of weakness in hypokalemic periodic paralysis. If successful this work has the potential to lead to improved therapy for patients.
Patients with muscle diseases known as channelopathies suffer from muscle stiffness and bouts of weakness. In this proposal we explore development of novel therapy for weakness in patients with the muscle channelopathy hypokalemic periodic paralysis.
