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Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative motoneuron (MN) where in fast fatigable motor units (MUs) of vulnerable motor pools preferentially degenerate followed by fast fatigue resistant and slow MUs . Excitability is a key endogenous mechanism of MN neuroprotection [1] and therefore we hypothesize that pre-symptomatic excitability indicates impending disease development. Using a transgenic mouse model for ALS, we performed in vitro patchclamp electrophysiology in ALS-vulnerable trigeminal motoneurons (TMNs) retrogradely labeled from jaw closer muscles at P8-12. We proposed a novel k-means clustering approach to classify TMNs into putative fast fatigable (PFF), fast fatigue resistant (PFR) and slow (PS) MUs based on rheobase and input resistance. Interestingly, hyper-excitability was noted in PFF and PFR

Early dysregulation of trigeminal motor pool excitability in a mouse model for neurodegenerative motoneuron disease