Title : Nicotine-induced neuroprotection against N-methyl-D-aspartic acid or beta-amyloid peptide occur through independent mechanisms distinguished by pro-inflammatory cytokines.

Pub. Date : 2003 Dec

PMID : 14622092






3 Functional Relationships(s)
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1 Nicotine-induced neuroprotection against different toxins is imparted through pharmacologically distinct neuronal nicotinic acetylcholine receptors (nAChR) where protection against chronic N-methyl-d-aspartic acid (NMDA) exposure is through nAChRalpha7 but protection against the toxic peptide of amyloid precursor protein, Abeta25-35, is through nAChRalpha4beta2. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
2 Nicotine-induced neuroprotection against different toxins is imparted through pharmacologically distinct neuronal nicotinic acetylcholine receptors (nAChR) where protection against chronic N-methyl-d-aspartic acid (NMDA) exposure is through nAChRalpha7 but protection against the toxic peptide of amyloid precursor protein, Abeta25-35, is through nAChRalpha4beta2. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
3 Therefore, the neuroprotective effects of nicotine against differing toxic assaults requires distinct nAChR subtypes and proceeds through intracellular pathways that overlap with similarly different mechanisms initiated by pro-inflammatory cytokines. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus