Figure 4.

Evidence for direct neurotransmission from adult-born GCs to mature GCs. A: Example traces of optically evoked IPSCs, before (black) and after (red) application of glutamate antagonists (10 µM NBQX, 100 µM DL-APV). B: NBQX/APV reduced IPSC amplitudes evoked by 50 ms stimuli by 75.1 ± 6.6 % (Control: 199.6 ± 48.8 pA, NBQX/APV: 38.2 ± 13.0 pA, n = 14; Paired t-test, P < 0.001) and by 2 ms stimuli (in a distinct cohort of cells) by 76.0 ± 6.4% (Control mean: 245.3 ± 60.2 pA, residual mean: 40.7 ± 8.2 pA, n = 10; Wilcoxon Signed Rank Test, P = 0.002). C: Current-voltage relationship for residual currents (after NBQX+APV application, n = 8, currents normalized to peak amplitude at +20mV). Inset, IPSCs evoked at −115, −85, −55, −25, +5 and +20 mV holding-potentials. D: Residual IPSCs were abolished by 1 µM TTX (left, n = 5) and by nominal 0 mM extracellular calcium (right, n =5). E: Representative trace of a an NMDA receptor-mediated current recorded at +40 mV (black) following blockade of AMPA and GABA_A receptors, 5/5 cells tested showed such currents (mean amplitude: 190.3 ± 28.1 pA). For comparison, an AMPA receptor-mediated current at −65 mV in control conditions is shown. The 2 forms of glutamatergic input did not correlate in amplitude (Spearman Rank Correlation, r² = 0.6, P = 0.35, n = 5).