ArticlePflugers Archiv : European journal of physiology2021
Clenbuterol-sensitive delayed outward potassium currents in a cell model of spinal and bulbar muscular atrophy.
Article in Pflugers Archiv : European journal of physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 6 citations in OpenAlex.
- Unveiling the effect of curcumin on ion channels of SBMA motoneuron-derived cells and human IPSC-derived neurons: initial electrophysiological findings.European biophysics journal : EBJ · 2026Article
- Therapeutic advances in spinal muscular atrophy: a review of clinical, safety, and economic considerations.Frontiers in pharmacology · 2026Review
- Article
- Nucleoporin Nup358 Downregulation Tunes the Neuronal Excitability in Mouse Cortical Neurons.Life (Basel, Switzerland) · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disease caused by polyglutamine (polyQ) expansions in the androgen receptor (AR) gene. SBMA is characterized by selective dysfunction and degeneration of motor neurons in the brainstem and spinal cord through still unclear mechanisms in which ion channel modulation might play a central role as for other neurodegenerative diseases. The beta2-adrenergic agonist clenbuterol was observed to ameliorate the SBMA phenotype in mice and patient-derived myotubes. However, the underlying molecular mechanism has yet to be clarified. Here, we unveil that ionic current alterations induced by the expression of polyQ-expanded AR in motor neuron-derived MN-1 cells are attenuated by the administration of clenbuterol. Our combined electrophysiological and pharmacological approach allowed us to reveal that clenbuterol modifies delayed outward potassium currents. Overall, we demonstrated that the protection provided by clenbuterol restores the normal function through the modulation of K
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