Title : Nicotine-induced phosphorylation of ERK in mouse primary cortical neurons: evidence for involvement of glutamatergic signaling and CaMKII.

Pub. Date : 2007 Oct

PMID : 17666046






4 Functional Relationships(s)
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1 Nicotine-induced ERK phosphorylation was inhibited by high concentrations of mecamylamine, however it was not blocked by other broad nicotinic acetylcholine receptor (nAChR) inhibitors (including hexamethonium and chlorisondamine) or nAChR subtype selective inhibitors (such as methyllycaconitine, alpha-bungarotoxin, dihydro-beta-erythroidine, and alpha-conotoxin Au1B). Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
2 Nicotine-induced ERK phosphorylation was inhibited by high concentrations of mecamylamine, however it was not blocked by other broad nicotinic acetylcholine receptor (nAChR) inhibitors (including hexamethonium and chlorisondamine) or nAChR subtype selective inhibitors (such as methyllycaconitine, alpha-bungarotoxin, dihydro-beta-erythroidine, and alpha-conotoxin Au1B). Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
3 Nicotine-induced ERK phosphorylation was inhibited by high concentrations of mecamylamine, however it was not blocked by other broad nicotinic acetylcholine receptor (nAChR) inhibitors (including hexamethonium and chlorisondamine) or nAChR subtype selective inhibitors (such as methyllycaconitine, alpha-bungarotoxin, dihydro-beta-erythroidine, and alpha-conotoxin Au1B). Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
4 In accord with these pharmacological results, nicotine-induced ERK phosphorylation was normal in primary cultures made from beta2 or alpha7 nAChR subunit knockout mice. Nicotine cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus