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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 2011 Mar 25;108(16):6689. doi: 10.1073/pnas.1104147108

Correction for Thompson et al., Transgenic elimination of high-affinity antidepressant and cocaine sensitivity in the presynaptic serotonin transporter

PMCID: PMC3081007

NEUROSCIENCE Correction for “Transgenic elimination of high-affinity antidepressant and cocaine sensitivity in the presynaptic serotonin transporter,” by Brent J. Thompson, Tammy Jessen, L. K. Henry, Julie R. Field, Karen L. Gamble, Paul J. Gresch, Ana M. Carneiro, Rebecca E. Horton, Peter J. Chisnell, Yekaterina Belova, Douglas G. McMahon, Lynette C. Daws, and Randy D. Blakely, which appeared in issue 9, March 1, 2011, of Proc Natl Acad Sci USA (108:3785–3790; first published January 31, 2011; 10.1073/pnas.1011920108).

The authors note that, due to a printer's error, on page 3787, right column, first paragraph, lines 8–20, “Although significant evidence supports a primary role for the 5-HT transporter in the reinforcing properties of psychostimulants (35–37), SERT blockade also appears to contribute to reinforcement (38–40). Indeed, SERT appears to be primarily responsible for the sustained reinforcing properties of cocaine in the 5-HT transporter–KO mouse (22, 23, 39–41). The significant compensatory alterations evident in 5-HT transporter–KO mice encouraged Chen and colleagues (42, 43) to develop a mouse bearing knock-in mutations in 5-HT transporter that, in vitro, reduced cocaine potency. Studies with these mice have yielded convincing evidence that 5-HT transporter is a key determinant of many synaptic and behavioral actions of cocaine” should instead appear as “Although significant evidence supports a primary role for the DA transporter in the reinforcing properties of psychostimulants (35–37), SERT blockade also appears to contribute to reinforcement (38–40). Indeed, SERT appears to be primarily responsible for the sustained reinforcing properties of cocaine in the DA transporter–KO mouse (22, 23, 39–41). The significant compensatory alterations evident in DA transporter–KO mice encouraged Chen and colleagues (42, 43) to develop a mouse bearing knock-in mutations in the DA transporter that, in vitro, reduced cocaine potency. Studies with these mice have yielded convincing evidence that the DA transporter is a key determinant of many synaptic and behavioral actions of cocaine.”


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