The ratio of caspase-3-activated
GC density in the D-domain to that in the V-domain was 1.5 ± 0.1 before food and 1.8 ± 0.1 in the postprandial period (Figure 6D), showing no significant difference between the Fulvestrant clinical trial two time points (p = 0.09). These results indicate that the deprivation of sensory input in the local OB area in ΔD mice greatly enhanced GC elimination in that local area during the postprandial period. An increase in apoptotic GCs in the D-domain of ΔD mice during the postprandial period was also confirmed by an increase in TUNEL-positive cells (Figure S5F). Disturbance of postprandial behaviors of ΔD mice suppressed the enhanced GC apoptosis 2 hr after the start of food supply in both the D- and V-domains (Figures 6E, 6F, and S5E). Apoptotic GCs in ΔD mice showed no significant
increase 1 hr after the start of food supply, as was also seen in wild-type mice with Bleomycin purchase intact nostrils (Figures 6E and 6F). In the D-domain of ΔD mice, more than half of caspase-3-activated GCs were either BrdU-positive (14–20 days of age) or DCX-positive new GCs both before and 2 hr after the start of food supply (Figures 6G and S5G). To examine whether enhanced apoptosis of new GCs in locally sensory-deprived areas leads to a decrease in their long-term survival in these areas, adult-born GCs were BrdU-labeled and followed-up for 2 months (Figures 6H–6K and S5H). In the ΔD mice OB, the total number of BrdU-labeled cells per OB on days 9–13 was 72.1% of that in wild-type mice OB (Figure S5I), reflecting the small volume of the ΔD mouse OB. Interestingly,
however, the density of labeled GCs in the D-domain of ΔD mice on days 9–13 was 1.7-fold larger than that in the the V-domain of these mice (Figures 6H and 6J), which was also larger than that in the D- and V-domains of wild-type mice (Figures 6I and 6J). In this period, the density of BrdU and DCX double-positive GCs remarkably increased in the D-domain of ΔD mice (Figure S5J), indicating the enhanced recruitment of immature GCs in the area. Labeled cell density in the D-domain of ΔD mice decreased remarkably thereafter, becoming comparable to that in the V-domain on days 28–32 and 56–60 (ratio, ∼1.0; Figures 6H and 6J). Survival rate of adult-born GCs (density ratio of BrdU-labeled cells, days 56–60/days 9–13) in the D-domain was 34.7%, which was significantly lower than that in the V-domain (62.3%; Figure 6K). In wild-type mouse OB, the density of labeled GCs in the D-domain was slightly higher than that in the V-domain, and the ratio (D-domain/V-domain) was constant across all time points examined (nearly 1.2; Figures 6I and 6J). Survival rates of adult-born GCs in the D- and V-domains of wild-type mice were comparable to that in the V-domain of ΔD mouse OB (Figure 6K). These results indicate the local regulation of (1) immature GC recruitment, (2) sensory input-dependent apoptosis of new GCs, and (3) long-term survival of new GCs, in the ΔD mouse OB.