Figure 8.

Action potential and membrane depolarization-induced [Ca²⁺]_i transients are attenuated by blocking L-type Ca²⁺ channels. A, Representative experiment showing the relationship of membrane voltage to Δ[Ca²⁺]_i in the soma and dendrites of an SCN neuron depolarized (10–100 pA) for 200 ms in the presence of TTX (0.5 μm). The L-type Ca²⁺ channel blocker nimodipine (20 μm) reduced the Δ[Ca²⁺]_i ∼40%. B, RHT-evoked action potential-induced [Ca²⁺]_i transients were attenuated by nimodipine (20 μm) in the presence of picrotoxin (50 μm). Ten stimulus pulses were applied to the RHT at the frequencies indicated before and after nimodipine treatment. During RHT stimulation, occasional stimuli failed to evoke an action potential or a spontaneous action potential occurred; therefore, to facilitate comparisons between experiments, the ΔCa²⁺ was normalized (estimated ΔCa²⁺ = ΔCa²⁺/#AP × 10). Nimodipine significantly reduced Ca²⁺ transients (mean with SEM) over a range of stimulus frequencies (1–20 Hz, n = 7 neurons; 0.5 Hz, n = 6 neurons; *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.005, paired t test). Est., Estimated.