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. 2021 Jan 19;131(2):e144450. doi: 10.1172/JCI144450

Figure 3. Magel2 deficiency decreases AVP receptor levels in SST neurons of the dorsal LS.

Figure 3

(A) Regional precision of 1 nM [125I]LVA binding without (total) and with (nonspecific) unlabeled AVP in excess on frozen brain sections of Magel2+/+ and Magel2+/–p mice. Data (mean ± SEM) expressed as a percentage relative to Magel2+/+ in n = 8 Magel2+/+ and 7 Magel2+/–p mice. Two-way ANOVA: genotype F1,26 = 2.08, P = 0.16; effect of subregions in LS F1,26 = 0.13, P = 0.71; post hoc Sidak test for comparisons. (B) Cellular precision of 50 μM d[Lys(Alexa Fluor 647)8]VP binding without (total, n = 4 mice) and with (nonspecific, n = 3 mice) 100 μM Manning compound injected directly into the LS of Magel2+/+ mice. OXTR competitor (5 μM TGOT, n = 5 mice) coinjected with d[Lys(Alexa Fluor 647)8]VP to specify AVPR binding sites representative of 3 independent experiments. Scale bar: 1 mm. Binding affinity for AVPR subtypes presented in Supplemental Table 1. (C) Coexpression of AVPR binding sites with the indicated markers. Arrows point to cells with “bright” labeling and arrowheads to cells with “dim” labeling. Scale bars: 25 μm. Percentage of cells coexpressing AVPR and cell markers are indicated. (D) Proportion of cell types with AVPR binding sites for d[Lys(Alexa Fluor 647)8]VP in dorsal LS. Data (mean ± SEM) expressed as percentage relative to Magel2+/+ in n = 6 Magel2+/+ and 6 Magel2+/–p mice. Three-way ANOVA for cell type F2,59 = 37.27, P < 0.0001; AVPR binding F1,59 = 49.85, P < 0.0001; genotype F1,59 = 1.83, P = 0.18; cell type × AVPR binding × genotype F2,59 = 5.35, P = 0.0073; post hoc Sidak test results as indicated.