Figure 3
From: Bidirectional regulation of emotional memory by 5-HT1B receptors involves hippocampal p11
Increased pre- and postsynaptic hippocampal glutamate neurotransmission by 5-HT1BR stimulation in p11KO mice. Glutamate-oxidase enzyme based MEA recordings of potassium-evoked glutamate release amplitudes in hippocampal CA1 and DG subregions of anesthetized mice (a). Real-time in vivo amperometric responses of reproducible glutamate dynamics recorded at 2 Hz, with glutamate recording sites (corresponding to responses in red and black) and sentinel or reference sites (corresponding to responses in blue and green) (b). Event markers indicated by arrows mark depolarization-induced responses evoked by 120 mM KCl with and without co-administration of 10 μM of CP94253 (b), with 60 s between each local application of KCl. For glutamate release amplitudes in the DG, an interaction was found between CP94253 and genotype (a). In the CA1, CP94253 resulted in a higher KCl-evoked glutamate release amplitude in P11KO mice compared to baseline depolarization-evoked release of glutamate in P11KO mice (a). Histograms quantifying total protein levels and phosphorylated form of the protein normalized to the total level of the protein (c–d) in the hippocampus. Representative western blots are shown above each histogram. Genotype-dependent effects were found for phosphorylation at Ser831 of the GluR1 subunit and increased phosphorylation at Ser845-GluR1 by CP94253 in p11KO mice (d). Data are presented as means±s.e.m. (a) 3–5 reproducible peaks with n=10–14 (DG) and 8–10 (CA1) recordings per group. (c–d) n=5–6. CA1: cornu ammonis 1 of hippocampus, DG: dentate gyrus of hippocampus, CP: CP94253 (5-HT1BR agonist), G: genotype, P11KO: p11 knock-out mice, WT: wild type mice, K: KCL (potassium chloride, 120 mM), MEA: microelectrode array. *P<0.05; **P<0.01.
