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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: Hippocampus. 2009 Sep;19(9):779–789. doi: 10.1002/hipo.20559

Figure 1. Low concentration of VIP (1nM) enhances NMDA-evoked peak currents in isolated CA1 pyramidal neurons and this effect is mediated by VPAC receptors.

Figure 1

A. Application of VIP (1nM) to acutely isolated CA1 pyramidal neurons increased NMDA-evoked peak currents (39 ± 4%, n=6, data obtained at 30 min of recording), it lasted throughout the recording period. But in the presence of 0.1μM [Ac-Tyr1, D-Phe2] GRF (1–29), a specific VPAC-R agonist, VIP effect on NMDA-evoked peak currents was inhibited (4 ± 2%, n = 6, data obtained at 30 min of recording). But the addition of 0.1μM M65, a specific PAC1-R antagonist, could not prevent the increase of NMDA-evoked currents (39 ± 7%, n = 5, data obtained at 30 min of recording). B. Sample traces from the same cells with VIP or VIP + [Ac-Tyr1, D-Phe2] GRF (1–29) or VIP + M65 in the bath solution are shown at baseline (t = 3min) and after drug application (t=28min). C. Addition of 10nM [Ala11,22,28]VIP, a VPAC1-selective agonist, caused an enhancement in NMDA-evoked currents (27 ± 2%, n=6, data obtained at 30 min of recording), but the existence of 0.1μM [Ac-Tyr1, D-Phe2] GRF (1–29) blocked the potentiation of NMDA-evoked currents (−7 ± 2%, n=5, data obtained at 30 min of recording) plus 10nM [Ala11,22,28]VIP. D. Application of 1nM Bay55-9837, a specific VPAC2-selective agonist, alone also increased NMDA evoked currents (44 ± 8%, n=6, data obtained at 30 min of recording), but the coapplication of 0.1μM [Ac-Tyr1, D-Phe2] GRF (1–29) with 1n1M Bay55-9837, has no effect on NMDA-evoked currents (4 ± 3%, n=5, data obtained at 30 min of recording).