Figure 7.

BDNF increased NMDA currents in DRG neurons. DRG neurons from adult rats were cultured for 2 or 3 days (A) without or (B–D) with ketamine (200 μM). Prior to whole-cell patch-clamp recording, cells were left untreated or were pre-treated for 1–2 h with BDNF (20 ng/ml), proBDNF (20 ng/ml) or BDNF plus ANA-12 (100 nM). Once the cells had stabilized at a holding potential of −70 mV under voltage-clamp conditions, NMDA (250 μM) and glycine (10 μM) were applied for 10 s by pressure ejection and the peak current measured. (A) Cells cultured without ketamine showed negligible currents in response to NMDA + Gly, independently of whether they were incubated with BDNF or not. (B) Cells cultured in ketamine responded to NMDA + Gly, and the currents were larger after incubation with BDNF. (C) In cells preincubated with BDNF, a first application of NMDA+Gly evoked a current that suppressed in a second application in the presence of the NMDA receptor antagonist AP-5 (50 μM) applied for 10 min. After washout of AP-5, a third application of NMDA+Gly evoked a current of the same amplitude as the first. (D) Pretreatment with BDNF (but not with proBDNF) increased the inward current induced by NMDA. The trkB antagonist ANA-12 eliminated the increase produced by BDNF. BDNF also increased the number of cells responding to NMDA (>50 pA): from 50 % in the untreated cohort (n = 25) to 95 % in the BDNF-treated cohort (n = 19). Horizontal lines indicate the mean and errors bars indicate the SEM. **P = 0.0094, Holm–Sidak’s post-test to one-way ANOVA.