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. 2014 Oct 3;1(11):851–866. doi: 10.1002/acn3.118

Figure 7.

Figure 7

Concurrent heterozygous GABABR1 KO blunted the ability of CaSR KO to protect neurons against ischemic injury. (A) TUNEL staining of hippocampi; (B) the % of neurons preserved; and (C) the % of TUNEL-(+) neurons shown in hippocampi in control (Cont), HippCaSR−/−, and HippCaSR−/−//GABABR1+/− mice subjected to TGI (15 min) and in HippCaSR−/−//GABABR1+/− mice subjected to Sham procedure, followed by 3 days of reperfusion. *P < 0.05; **P < 0.01 versus TGI-treated Cont mice; #P < 0.01 versus HippCaSR−/− mice, N = 6–8 mice/group. Scale bar: 20 μm. (D) Representative immunohistochemical staining for the expression of GABABR1 in hippocampi of control (Cont), HippCaSR−/−, and HippCaSR−/−//GABABR1+/− mice subjected to TGI procedure, followed by 3 days of reperfusion. N = 6–8 mice/group. Scale bar: 20 μm. GABABR1, γ-aminobutyric acid receptor 1; KO, knockout; CaSR, Ca2+-sensing receptor; TUNEL, transferase dUTP nick end-labeling; TGI, transient global ischemia.