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. 2013 Sep 17;7:157. doi: 10.3389/fncel.2013.00157

FIGURE 2.

FIGURE 2

D2R signaling pathways activated in response to seizures. (A) Pattern of c-fos mRNA induction (dark staining) in the brain of WT and D2R-/- mice treated with 10, 20, and 35 mg/kg kainic acid (KA), as indicated. Brains were dissected 3 h after KA administration and coronal sections were processed by mRNA in situ hybridization with a c-fos specific anti-sense riboprobe (see Bozzi et al., 2000 for experimental details). Administration of 20 mg/kg KA induced limbic motor seizures in D2R-/- but not WT mice (Bozzi et al., 2000; Tripathi et al., 2010; Dunleavy et al., 2013), whereas generalized seizures were observed in both genotypes at 35 mg/kg KA (Bozzi et al., 2000). (B,C) Induction of ERK phosphorylation (pERK) and c-Fos protein synthesis in the hippocampus of WT and D2R-/- mice following KA-induced seizures. Mice received a single systemic dose of KA (20 mg/kg) and ERK/pERK (B) and c-Fos (C) induction were analyzed by immunoblotting on total hippocampal protein extracts at different times after KA (1, 3, and 6 h, as indicated). CA3, pyramidal cell layer of the hippocampus; D2R-/-, D2R knockout mice; KA, kainic acid; (p)ERK, (phosphorylated) extracellular-regulated kinase; saline, saline-treated mice; WT, wild-type mice.

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