Michael J. Marks
Institute for Behavioral Genetics
447 UCB
University of Colorado
1480 30th St.
USA
Name/email consistency: high
- Increased nicotinic acetylcholine receptor protein underlies chronic nicotine-induced up-regulation of nicotinic agonist binding sites in mouse brain. Marks, M.J., McClure-Begley, T.D., Whiteaker, P., Salminen, O., Brown, R.W., Cooper, J., Collins, A.C., Lindstrom, J.M. J. Pharmacol. Exp. Ther. (2011)
- 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. Marks, M.J., Meinerz, N.M., Drago, J., Collins, A.C. Neuropharmacology (2007)
- Deletion of the alpha7, beta2, or beta4 nicotinic receptor subunit genes identifies highly expressed subtypes with relatively low affinity for [3H]epibatidine. Marks, M.J., Whiteaker, P., Collins, A.C. Mol. Pharmacol. (2006)
- Subsets of acetylcholine-stimulated 86Rb+ efflux and [125I]-epibatidine binding sites in C57BL/6 mouse brain are differentially affected by chronic nicotine treatment. Marks, M.J., Rowell, P.P., Cao, J.Z., Grady, S.R., McCallum, S.E., Collins, A.C. Neuropharmacology (2004)
