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. 2023 Jun 20;12:e79648. doi: 10.7554/eLife.79648

Figure 1. The α1AR agonist phenylephrine (PHE) augments NPo of L-type Ca2+ channels (LTCCs) in hippocampal neurons.

Figure 1.

(A) Neurons were preincubated with vehicle, PHE and prazosin (PRAZ) before seal formation. (B) Ten consecutive traces from representative cell-attached single-channel recordings of LTCCs from cultured hippocampal neurons with vehicle (water; black), 10 µM PHE (red), PHE plus 20 nM prazosin (bright green), and prazosin alone (dark green). (C) The increase in NPo by PHE was blocked by prazosin. F3,40 = 5.474. Control vs. PHE, p = 0.0036; PHE vs. Prazosin + PHE, p = 0.0334; Control vs. Prazosin only, p = 0.9723. (D) Ensemble averages during depolarization. (E) The increase in ensemble average peak currents by PHE was blocked by prazosin. F3,40 = 4.506. Control vs. PHE, p = 0.0101; PHE vs. Prazosin + PHE, p = 0.0316; Control vs. Prazosin only, p = 0.9722. (C, E) Data are presented as means ± standard error of the mean (SEM). n represents the number of cells (*p ≤ 0.05, **p ≤ 0.01; analysis of variance [ANOVA] with post hoc Holm–Sidak’s multiple comparisons test). Panel A was created using Biorender.com.