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Shortening of action potential duration in HL‐1 cells following rapid electrical stimulation. (A) Representative action potential traces recorded from HL‐1 cells under control conditions and after 2 days of rapid pacing at 300 bpm; the recording frequency was 1 Hz. (B) Summary of APD 90 measurements at different stimulation frequencies, comparing control and paced groups. (C) Representative I Ca, L traces recorded via patch clamp, with voltage steps initiated from −90 mV (left) and −40 mV (right). (D) Dose–response curves of L‐type calcium current inhibition by varying concentrations of <t>nimodipine.</t> (E) Current–voltage (I–V) relationships under different holding potentials (−90 mV and −40 mV), illustrating voltage dependence. All experiments were repeated in triplicate ( n = 3 biological replicates). * p < 0.05.
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Shortening of action potential duration in HL‐1 cells following rapid electrical stimulation. (A) Representative action potential traces recorded from HL‐1 cells under control conditions and after 2 days of rapid pacing at 300 bpm; the recording frequency was 1 Hz. (B) Summary of APD 90 measurements at different stimulation frequencies, comparing control and paced groups. (C) Representative I Ca, L traces recorded via patch clamp, with voltage steps initiated from −90 mV (left) and −40 mV (right). (D) Dose–response curves of L‐type calcium current inhibition by varying concentrations of <t>nimodipine.</t> (E) Current–voltage (I–V) relationships under different holding potentials (−90 mV and −40 mV), illustrating voltage dependence. All experiments were repeated in triplicate ( n = 3 biological replicates). * p < 0.05.
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Shortening of action potential duration in HL‐1 cells following rapid electrical stimulation. (A) Representative action potential traces recorded from HL‐1 cells under control conditions and after 2 days of rapid pacing at 300 bpm; the recording frequency was 1 Hz. (B) Summary of APD 90 measurements at different stimulation frequencies, comparing control and paced groups. (C) Representative I Ca, L traces recorded via patch clamp, with voltage steps initiated from −90 mV (left) and −40 mV (right). (D) Dose–response curves of L‐type calcium current inhibition by varying concentrations of nimodipine. (E) Current–voltage (I–V) relationships under different holding potentials (−90 mV and −40 mV), illustrating voltage dependence. All experiments were repeated in triplicate ( n = 3 biological replicates). * p < 0.05.

Journal: Journal of Cell Communication and Signaling

Article Title: P2X7 receptors promote atrial remodeling and atrial fibrillation susceptibility via reactive oxygen species‐mediated mitogen‐activated protein kinase signaling activation

doi: 10.1002/ccs3.70071

Figure Lengend Snippet: Shortening of action potential duration in HL‐1 cells following rapid electrical stimulation. (A) Representative action potential traces recorded from HL‐1 cells under control conditions and after 2 days of rapid pacing at 300 bpm; the recording frequency was 1 Hz. (B) Summary of APD 90 measurements at different stimulation frequencies, comparing control and paced groups. (C) Representative I Ca, L traces recorded via patch clamp, with voltage steps initiated from −90 mV (left) and −40 mV (right). (D) Dose–response curves of L‐type calcium current inhibition by varying concentrations of nimodipine. (E) Current–voltage (I–V) relationships under different holding potentials (−90 mV and −40 mV), illustrating voltage dependence. All experiments were repeated in triplicate ( n = 3 biological replicates). * p < 0.05.

Article Snippet: Nimodipine (HY‐10350) was obtained from MedChemExpress (MCE, USA), prepared in 0.1% dimethyl sulfoxide (DMSO) as a stock solution, and then diluted to the desired concentrations for experimental use.

Techniques: Control, Patch Clamp, Inhibition

Cells were pretreated without or with IGF-1 (10 ng/mL) followed by the L-type calcium channel blocker nimodipine (5 µM) and the NMDAR antagonist APV (50 µM). After 3 minutes, they were stimulated with AMPA. Representative traces show that IGF-1 attenuates AMPA-evoked [Ca 2+ ] i elevation ( P <0.05; Student’s t test) independent of L-type calcium channels.

Journal: bioRxiv

Article Title: Insulin Growth Factor 1 affects glutamate receptor activity differently in primary cultures of neocortical versus hippocampal neurons

doi: 10.64898/2026.04.04.716504

Figure Lengend Snippet: Cells were pretreated without or with IGF-1 (10 ng/mL) followed by the L-type calcium channel blocker nimodipine (5 µM) and the NMDAR antagonist APV (50 µM). After 3 minutes, they were stimulated with AMPA. Representative traces show that IGF-1 attenuates AMPA-evoked [Ca 2+ ] i elevation ( P <0.05; Student’s t test) independent of L-type calcium channels.

Article Snippet: In the pharmacological isolation of evoked currents, the drugs used included the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; Tocris) and nimodipine (Tocris), an L-type calcium channel blocker, dissolved in dimethyl sulfoxide (DMSO) to create a stock solution, ensuring the final DMSO concentration was below 0.05%.

Techniques: