Skip to main content
. Author manuscript; available in PMC: 2015 May 7.
Published in final edited form as: Neuron. 2014 May 7;82(3):645–658. doi: 10.1016/j.neuron.2014.03.028

Fig. 2. FMRP-deficient mice have cocaine reward deficits that relate to mGluR5 hyperactivity and not to general deficits in natural reward processes or learning/memory.

Fig. 2

(A) Timeline for CPP (C=COC, S=SAL). (B) Fmr1 KO mice show significantly decreased preference for a COC-paired context (7.5 mg/kg; n=11 WT, 12 KO). (C) Assessment of learning and memory in Fmr1 KO and WT mice using fear conditioning shows no differences in training, contextual or cued testing (n=11 KO, 12 WT). (D) Timeline for food CPP (HF=high fat, RC=regular chow). (E) Fmr1 KO and WT littermates show comparable preference for high fat chow (n=16 KO, 15 WT). (F) They also do not differ in two-bottle choice preference for sucrose (n=10 KO, 10 WT). (G) Compound mutant littermates show that impaired CPP in total Fmr1KO mice is rescued by a reduction in the mGluR5 receptor (n=29 WT/WT, 27 HET/WT, 22 WT/KO, 27 HET/KO). Asterisk in G indicates significant follow-up Bonferroni post-hoc test. (* p<0.05, ** p<0.01, *** p<0.001; data shown are mean±S.E.M.; see also Table S1 & Fig. S2.)