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Fig. 5. Expression and contribution of neurotransmitter receptors in the BDNF-overexpressing hippocampus. (A) Western blot analysis of the GABAA receptor {alpha}1 subunit and the glutamate receptor NR1, NR2A, GluR1 and GluR2/3 subunits in membrane fractions isolated from wild-type (C) and transgenic (BDNF) forebrains at E18. There are no differences between groups. (B-G) Immunostaining for the GABAA {alpha}2 (B,E), NR1 (C,F) and GluR2/3 subunits (D,G) in control (B-D) and BDNF-overexpressing (E-G) E18 hippocampal sections. These subunits are distributed in a similar way throughout the hippocampal formation of control and transgenic embryos. In addition, no major changes in the density of immunostaining were observed. (H,I) Representative paired correlation maps showing spontaneous correlated network activity in the CA1 region of a transgenic hippocampal slice before (H) and after (I) blocking GABAA receptors by administration of 30 µM BMI. Note that GABAA receptor blockade decreases correlated network complexity. (J-L) Histograms showing the percentage of active neurons (J), the activation rate (K) and the number of active cells in spontaneous correlated networks (L) in the E18 CA1 region after incubations with the GABAA, NMDA and AMPA/kainate antagonists BMI, APV and CNQX, respectively. Data are stardardized to baseline values. White bars represent wild-type and black bars, transgenic embryos. The number of slices used ranged from 3 to 10 for each experimental condition. BMI incubation blocks spontaneous network activity in both wild-type and transgenic slices. Data are mean ± s.e.m. Significance levels: *P<0.05, **P<0.01, Student t-test. Scale bars, 200 µm. Abbreviations as in Fig. 1.





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