Skip to main content
. Author manuscript; available in PMC: 2010 Jan 1.
Published in final edited form as: Nat Neurosci. 2009 Nov 15;13(1):76–83. doi: 10.1038/nn.2447

Figure 6.

Figure 6

No schizophrenia-related phenotypes were observed following adult NR1 deletion. (a) Left, representative photomicrographs from cortex of the adult knockout mutant (Ppp1r2-cre+/−; NR1loxP/loxP-line B) prior to onset of recombination (8 weeks old) and after recombination was completed (20 weeks old). Brown arrows indicate colocalization of Gad67 and NR1 mRNAs, and red arrows indicate GAD67-positive neurons lacking NR1 mRNA. Right, quantification of double in situ hybridization detection of NR1 and Gad67 mRNA in the adult knockout mutants (n = 3 for each age). (b,c) Single-housed adult knockout mutants tested at 25–29 weeks of age were not impaired in a social-recognition test (b) or PPI (c). (d) After crossing with the loxP-flanked Rosa26-EYFP mice, adult knockout mutants (Ppp1r2-cre+/−; NR1loxP/loxP-line B; Rosa26-EYFPloxP/+) showed no significant change in GAD67 or parvalbumin immunoreactivity in Cre-targeted neurons of layer II/III S1 compared to Cre controls (Ppp1r2-cre+/−; Rosa26-EYFPloxP/+) at 26–27 weeks old. T, Cre-targeted neurons; Non-T, nontargeted neurons. Data are mean ± s.e.m.; n is indicated in parentheses.