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. Author manuscript; available in PMC: 2014 Aug 1.
Published in final edited form as: Neuropharmacology. 2013 Apr 12;71:191–203. doi: 10.1016/j.neuropharm.2013.03.038

TABLE 2.

Effect of the 6-OHDA lesion on α6β2* nAChRs and α4β2* nAChRs in rat striatum. 125I-Epibatidine binding in the presence of the α6β2* nAChR antagonist α-CtxMII was used to identify α4β2* nAChRs, while 125I-α-CtxMII was used to detect α6β2* nAChRs in striatum. The concentrations of 125I-α-CtxMII and 125I-epibatidine were 0.5 nM and 0.015 nM, respectively. Values represent the mean ± SEM of 8 rats 6-OHDA-lesioned rats not treated with nAChR drugs.

nAChRs fmol/mg tissue
% Control
Unlesioned side Lesioned side
α6β2* 3.45 ± 0.13 0.10 ± 0.01*** 2.9
α4β2* 6.86 ± 0.23 6.08 ± 0.03* 88

Significance of difference from unlesioned side:

*

p < 0.05,

***

p < 0.001.