Nicotinic receptors modulate the onset of reactive oxygen species production and mitochondrial dysfunction evoked by glutamate uptake block in the rat hypoglossal nucleus
Glutamate uptake block evokes hypoglossal motoneuron damage due to excitotoxicity. Reactive oxygen species are the earliest excitotoxic players for oxidative damage. Mitochondrial energy deficit is manifested later. Intrinsic cholinergic transmission is inadequate to arrest these events. Nicotinic receptor activation by nicotine provides strong neuroprotection.