Figure 3.

CaSR KO protected neurons from ischemic injury and restored GABA_BR1 expression in hippocampi of ^HippCaSR^−/− mice. (A) Representative H&E-stained sections of hippocampi; (B) the % of neurons (normalized to the numbers of neurons in Sham-treated Cont mice) which were preserved; (C) representative TUNEL staining of hippocampi; (D) the percentage of TUNEL-(+) neurons normalized to neuronal numbers acquired from adjacent sections stained with H&E as represented in (A) which were shown; and (E) expression of GABA_BR1 protein, as assessed by immunohistochemistry, in 6 months old control (Cont) and ^HippCaSR-KO mice subjected to TGI (15 min) or Sham procedures. *P < 0.01 versus Sham in each animal group; #P < 0.01 versus TGI-Cont mice in (B); *P < 0.05, **P < 0.01 versus TGI-Cont in (D). Mean ± SE, N = 6–12 mice/group. Scale bar: 20 μm. CaSR, Ca²⁺-sensing receptor; KO, knockout; GABA_BR1, γ-aminobutyric acid receptor 1; TUNEL, transferase dUTP nick end-labeling; TGI, transient global ischemia.