Genetic deficiency of β2-containing nicotinic receptors attenuates brain injury in ischemic stroke

Highlights • Genetic deficiency of β2-nAChRs attenuates brain infarction and neurological deficit in ischemic stroke. • Pharmacological inhibition of β2-nAChRs attenuates brain infarction and neurological deficit in ischemic stroke. • Neuroprotection of β2-nAChRs ablation involves the reduction of g...

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Veröffentlicht in:	Neuroscience 2014-01, Vol.256, p.170-177
Hauptverfasser:	Liu, Q, Tang, Z, Gan, Y, Wu, W, Kousari, A, La Cava, A, Shi, F.-D
Format:	Artikel
Sprache:	eng
Schlagworte:	Action Potentials - drug effects Action Potentials - genetics Animals Biological and medical sciences Brain Injuries - drug therapy Brain Injuries - etiology Brain Injuries - genetics Cells, Cultured Cerebral Cortex - cytology Dihydro-beta-Erythroidine - pharmacology Dihydro-beta-Erythroidine - therapeutic use Disease Models, Animal Fundamental and applied biological sciences. Psychology Glucose - deficiency Hypoxia - physiopathology Infarction, Middle Cerebral Artery - complications Infarction, Middle Cerebral Artery - genetics L-Lactate Dehydrogenase - metabolism Magnetic Resonance Imaging Male Medical sciences Mice Mice, Knockout Neurologic Examination Neurology Neuroprotective Agents - pharmacology Receptors, Nicotinic - deficiency Receptors, Nicotinic - genetics Time Factors Vascular diseases and vascular malformations of the nervous system Vertebrates: nervous system and sense organs
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Zusammenfassung:	Highlights • Genetic deficiency of β2-nAChRs attenuates brain infarction and neurological deficit in ischemic stroke. • Pharmacological inhibition of β2-nAChRs attenuates brain infarction and neurological deficit in ischemic stroke. • Neuroprotection of β2-nAChRs ablation involves the reduction of glutamate-mediated excitotoxicity. • Inhibition of β2-nAChR in stroke could provide beneficial effects against ischemic brain injury.
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2013.10.049