Neuroscience, 2013-06, Vol.240, p.129-134
2013
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- Autor(en) / Beteiligte
- Titel
- Lack of sigma-1 receptor exacerbates ALS progression in mice
- Ist Teil von
- Neuroscience, 2013-06, Vol.240, p.129-134
- Ort / Verlag
- Amsterdam: Elsevier Ltd
- Erscheinungsjahr
- 2013
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0306-4522eISSN: 1873-7544DOI: 10.1016/j.neuroscience.2013.02.035Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3665351
- Format
- –
- 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