Lack of sigma-1 receptor exacerbates ALS progression in mice

Highlights ► Knockout of S1R in the SOD1G93A mouse model of ALS significantly reduces longevity. ► MN of mice lacking S1R exhibit increased excitability. ► S1R acts as a brake on excitability, an effect that might enhance longevity in an ALS mouse model.

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Bibliographische Detailangaben
Veröffentlicht in:	Neuroscience 2013-06, Vol.240, p.129-134
Hauptverfasser:	Mavlyutov, T.A, Epstein, M.L, Verbny, Y.I, Huerta, M.S, Zaitoun, I, Ziskind-Conhaim, L, Ruoho, A.E
Format:	Artikel
Sprache:	eng
Schlagworte:	Action Potentials - genetics Action Potentials - physiology ALS Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - metabolism Animals Animals, Newborn Biological and medical sciences Biophysics C-terminals Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Disease Progression Electric Stimulation excitability Green Fluorescent Proteins - genetics Homeodomain Proteins - genetics In Vitro Techniques Kv2.1 Longevity Medical sciences Mice Mice, Inbred C57BL Mice, Knockout motor neurons Mutation - genetics Neurology Neurons - metabolism Neurons - physiology Patch-Clamp Techniques Receptors, sigma - deficiency Receptors, sigma - genetics Sigma-1 Receptor Spinal Cord - pathology Superoxide Dismutase - genetics Swimming - psychology Transcription Factors - genetics
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Beschreibung
Zusammenfassung:	Highlights ► Knockout of S1R in the SOD1G93A mouse model of ALS significantly reduces longevity. ► MN of mice lacking S1R exhibit increased excitability. ► S1R acts as a brake on excitability, an effect that might enhance longevity in an ALS mouse model.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2013.02.035