Homozygotes are devoid of the nine H2-Mv cluster genes, yet immunohistochemistry does not detect any compensatory increase in expression of MHC class I genes in the basal vomeronasal epithelium. The accessory olfactory bulb appears to develop normally, the tripartite layering of the vemeronasal epithelium is reasonably normal, but there is a minor decrease in the number of basal vomeronasal sensory neurons (VSN) in 10-week-old males. NanoString analysis at 3 weeks of age shows no difference in RNA expression in 37 different vomeronasal receptors, and at 8 weeks of age only a small reduction in expression of 3 out of 36 receptors: Vmn2r10, Vmn2r14, and Vmn2r70. Vmn2r81-expressing VMNs, which normally co-express H2-Mv, have a decreased sensitivity to two separate peptide ligands; Vmn2r26-expressing VMNs, which normally do not co-express H2-Mv, do not show this decreased sensitivity to stimulation. Although Vmn2r81-expressing VMNs show reduced ligand sensitivity, with higher ligand concentration they can still respond at the same maximum level. A diminished sensitivity was also found to stimulation from the high molecular weight fraction of C57BL/6 male urine and to exocrine gland secreted peptide 1. Both homozygous males and homozygous lactating females show decreased aggression toward a castrated intruder male that had been swabbed with high molecular weight fraction of male urine. This diminished aggression can be restored to approximately normal levels by increasing 4 fold the dose of male urine applied to the intruder. Although homozygous males show no change in latency to mount, and homozygous females show no change in duration of investigation of the male anogenital region, homozygous females do display diminished lordosis behavior.
