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. 2015 Aug 25;7(4):1759091415598292. doi: 10.1177/1759091415598292

Figure 5.

Figure 5.

Y1 receptor activation decreases NMDA-stimulated RGC spiking activity. (a) Representative recordings of RGC spiking activity in ex vivo retina using MEA. Note the increase in spiking rate upon 30 µM NMDA. After washout of first NMDA stimulus, 1 µM (Leu31, Pro34) − NPY was applied for 10 min followed by a second NMDA stimulus. (b) The Delta 2 (second stimulus)/Delta 1 (first stimulus) ratios are presented for different drug applications, for 10 min, between NMDA stimuli: 1 µM NPY, 1 µM (Leu31, Pro34) − NPY, 1 µM NPY13–36, 1 µM (Gly1, . . . Aib32)-PP, or a drug-free solution (control). The application of (Leu31, Pro34) − NPY was able to reduce the NMDA-stimulated RGC spiking activity. This effect was blocked by the Y1 receptor antagonist BIBP 3226 (1 µM). (c) Percentage of RGCs presenting Delta 2/Delta 1 ratio below 0.9. The application of (Leu31, Pro34) − NPY significantly increased the percentage of cells with Delta 2/Delta 1 ratio below 0.9. BIBP 3226 was able to block the effect of (Leu31, Pro34) − NPY confirming the involvement of Y1 receptor activation. Data are presented as mean ± SEM of n = 3 to 10 independent experiments. **p < .01, compared with control; #p < .05, compared with (Leu31, Pro34) − NPY. Kruskal-Wallis followed by Dunn’s test.