Postnatal changes in the slow Ca2+ current (I-Ca(L)) were investigated in f
reshly isolated ventricular myocytes from neonatal (1-7 days old) and adult
(2-4 months old) rats, using whole-cell voltage clamp and single-channel r
ecordings. The membrane capacitance (mean +/- SEM) averaged 23.2 +/- 0.5 pF
in neonates (n = 163) and 140 +/- 4.1 pF in adults (n = 143). Ica(L) was m
easured as the peak inward current at a test potential of +10 mV (or +20 mV
) by applying a 300-ms pulse from a holding potential of -40 mV; 1.8 mM Ca2
+ was used as charge carrier. The basal ICa(L) density was 6.7 +/- 0.2 pA/p
F in neonatal and 7.8 +/- 0.2 pA/pF in adult cells (p < 0.05). The time cou
rse of inactivation of the fast component (at +10 ms) was significantly lon
ger in the neonatal (10.7 +/- 1.4 ms) than in the adult (6.6 +/- 0.4 ms) ce
lls (p < 0.05). Ryanodine (10 mu M) significantly increased this value to 1
8.0 +/- 1.9 in neonate (n = 8) and to 17.7 +/- 2.0 in adult (n = 9). For st
eady-state inactivation, the half-inactivation potential (V-h) was not chan
ged in either group. For steady-state activation, V-h was 5.1 mV in the neo
natal (n = 6) and -7.9 mV in the adult cells (n = 7). Single-channel record
ings revealed that long openings (mode-2 behavior) were occasionally observ
ed in the neonatal cells (11 events from 1080 traces/11 cells), but not in
the adult cells (400 traces/4 cells). Slope conductance was 24 pS in both t
he neonatal and adult cells. Results in rat ventricular myocytes suggest th
e following: (i) the peak Ca2+ current density is already well developed in
the neonatal period (being about 85% of the adult value); (ii) the fast co
mponent of inactivation is slower in neonates than in adults; and (iii) nat
urally occurring long openings are occasionally observed in the neonatal st
age but not in the adult. Thus, the L-type Ca2+ channels of the neonate wer
e slightly lower in density, were inactivated more slowly, and occasionally
exhibited mode-2 behavior as compared with those of the adult.