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. 1998 Aug 18;95(17):10235–10239. doi: 10.1073/pnas.95.17.10235

Figure 3.

Figure 3

Glutamate responsiveness is enhanced by BDNF, but not NT-3 or NGF. BDNF-induced increase in synaptic activity is blocked by NMDA receptor antagonism. (A) Example traces of control response to glutamate iontophoresis (10 ms pulse) and response after 20 min of NT-3 exposure. (B) Time course of mean effect of NT-3 on glutamate responses. (C) Group data for effects of heat-inactivated BDNF (HI-BDNF; P > 0.1; n = 3), BDNF (P < 0.01; n = 7), NGF (P > 0.4; n = 10), and NT-3 (P > 0.1; n = 11) on glutamate responsiveness. (D) Example traces of baseline synaptic activity and activity after 20 min of BDNF exposure, in the presence or absence of the NMDA receptor antagonist MK-801 (10 μM). (E) Group data for effect of BDNF on synaptic charge in the absence (P < 0.01; n = 11) or presence (P > 0.3; n = 7) of MK-801.