Abstract
The present study demonstrated that administration of nicotine prevented glutamate-induced motor neuronal death in primary cultures of the rat spinal cord. The nicotine-induced neuroprotection was inhibited by either dihydro-β-erythroidin (DHβE) or α-bungarotoxin (αBT), suggesting that it is mediated through both α4β2 and α7 nicotinic acetylcholine receptors (nAChRs). Both α4β2 and α7 nAChRs were identified on rat spinal motor neurons by immunohistochemical methods. We also demonstrated that galantamine, an acetylcholinesterase inhibitor with allosteric nAChR-potentiating ligand properties, prevented glutamate-induced motor neuronal death. These results suggest that stimulation of nAChR may be used as a treatment for ALS.
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