Axotomy and Target Deprivation Model in Mice

A unilateral occipital cortex ablation was the model for producing axotomy and target deprivation of dLGN neurons in mouse. Cortical ablations were done on adult (6–8 weeks old) male mice. For experiments on wild-type mice the C57BL/6J strain was used. For experiments on mice with NOS gene deletions, mice deficient in nNOS (B6;129S4-Nos1^tm1Plh/J, The Jackson Laboratory) and iNOS (B6;129P-Nos2^tm1Lau) were used. B6129SF2/J mice were controls for nNOS^−/− mice. B6129PF2/J mice were controls for iNOS^−/− mice. Two different lines of cyclophilin D null (ppif^−/−) mice were used: one line on a SV129 genetic background (Baines et al., 2005 (link); Martin et al., 2009a ) and another line on a C57BL/6 genetic background (Basso et al., 2005 (link)). Mouse cohort sizes were 6–10/genotype. The institutional Animal Care and Use Committee approved the animal protocols. The validation and reproducibility of this model of neuronal apoptosis in mouse has been described (Martin et al., 2002; Martin et al., 2003 (link); Natale et al., 2002 (link)). For corroboration of findings, an alternative model of pure target deprivation by excitotoxic lesioning was used (Portera-Cailliau et al., 1997b (link); Mueller et al., 2005 (link)). Unilateral visual cortical ablations were done on adult (6–8 weeks old) male mice using direct cortical injection of the N-methyl-D-aspartate (NMDA) receptor agonist quinolinic acid (QA, Sigma, St. Louis, MO) at a concentration of 60 nmol (500 nl total volume at 4 sites) dissolved in phosphate-buffered saline (PBS). Control mice received visual cortical injections of an equal volume of PBS.