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. 2021 Jun 1;10:e66612. doi: 10.7554/eLife.66612

Figure 7. preNMDARs contribute significantly to BDNF release following repetitive activity.

(A) Representative images showing expression of BDNF-pHluorin in the DG and CA3 area (arrows indicate mf axon, arrowheads indicate mf boutons). Control images (top), Grin1-cKO images (bottom). (B) Representative images of BDNF-pHluorin signal intensity at baseline and after repetitive stimulation of mfs (125 pulses, 25 Hz, ×2). Control images (left), Grin1-cKO images (right), arrowhead indicates region of interest. (C) Time course of BDNF-pHluorin signal intensity measured as ΔF/F (%): control (black), Grin1-cKO (red), Naïve (blue). (D) Quantification of BDNF-pHluorin signal in (C) during the last 100 s reveals larger BDNF release in control animals as compared to Grin1-cKO (control −18% ± 3%, n = 9 slices, five animals; Grin1-cKO −8 ± 1%, n = 10 slices, five animals; Grin1-cKO vs control, p=0.00648, unpaired t-test). Data are presented as mean ± s.e.m. **p<0.01.

Figure 7.

Figure 7—figure supplement 1. preNMDARs contribute significantly to BDNF release following a more physiological pattern of burst stimulation.

Figure 7—figure supplement 1.

(A) Representative images of BDNF-pHluorin signal intensity at baseline and after burst stimulation of mfs (5 pulses, 100 Hz, ×50, every 0.5 s). Control images (left), Grin1-cKO images (right), arrowhead indicates region of interest. (B) Time course of BDNF-pHluorin signal intensity measured as ΔF/F (%): control (black), Grin1-cKO (red), Naïve (blue). (C) Quantification of BDNF-pHluorin signal in (B) during the last 100 s reveals larger BDNF release in control animals as compared to Grin1-cKO (control −8.9% ± 2%, n = 7 slices, five animals; Grin1-cKO −3.5 ± 1%, n = 11 slices, five animals; Grin1-cKO vs control, p=0.0305, unpaired t-test). Data are presented as mean ± s.e.m. *p<0.05.