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. 2024 Nov 1;28(6):569–576. doi: 10.4196/kjpp.2024.28.6.569

Fig. 3. In the presence of D-APV, the NE-rescued LTP was abolished by.

Fig. 3

β1-AR antagonist. (A) In the presence of D-APV (50 µM), representative whole-cell recording traces showing paired-pulse stimulation (duration: 0.2 msec, interval: 50 msec) evoked EPSCs in PVN MNCs before (pre), after (post) delivering HFS during treatment with NE (100 nM; left) and a mixture of NE (100 nM) + CGP 20712 (1 µM). (B) In the presence of D-APV, pooled data showing the time course of normalized amplitude of N1 before and after the delivery of HFS (arrow head) during treatment with NE and a mixture of NE + CGP 20712. (C, D) Bar graphs show the normalized amplitude of N1 (C) and N2/N1 ratio (D) in each group, before (pre) and after (post) the delivery of HFS. D-APV, D-(-)-2-Amino-5-phosphonopentanoic acid; NE, norepinephrine; LTP, long-term potentiation; AR, adrenergic receptor; EPSCs, excitatory postsynaptic currents; PVN, paraventricular nucleus; MNCs, magnocellular neuroendocrine cells. *p < 0.05 vs. pre; #p < 0.05 vs. post of control; n = 8 cells from 6 mice in each group.