Title : Gene targeting demonstrates that alpha4 nicotinic acetylcholine receptor subunits contribute to expression of diverse [3H]epibatidine binding sites and components of biphasic 86Rb+ efflux with high and low sensitivity to stimulation by acetylcholine.

Pub. Date : 2007 Sep

PMID : 17631923






3 Functional Relationships(s)
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1 [3H]Epibatidine binds to nAChR subtypes in mouse brain with higher (KD approximately 0.02 nM) and lower affinity (KD approximately 7 nM), which can be further subdivided through inhibition by selected agonists and antagonists. Tritium cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
2 Deletion of the alpha7, beta2 or beta4 nicotinic receptor subunit genes identifies highly expressed subtypes with relatively low affinity for [3H]epibatidine. Tritium cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus
3 Deletion of alpha4 virtually eliminated cytisine-sensitive, higher-affinity [3H]epibatidine binding as did beta2 deletion, confirming that these sites are alpha4beta2*-nAChR. Tritium cholinergic receptor, nicotinic, alpha polypeptide 7 Mus musculus