Pregnant rats received saline once daily (Control QD) or twice daily (Control BID), cocaine 2 mg/kg IV daily (COC QD) or twice daily (COC BID) throughout gestation beginning on gestational day 4. The treatment was continued in nursing mothers until postnatal day 7. All studies were performed in their offsprings on postnatal days 1 and 7. An age-dependent increase in heart rate was observed from D1 to D7 in all four groups of animals. Cocaine exposure significantly increased heart rate in the once daily treatment group on D1 and D7. In contrast, twice daily cocaine exposure did not alter heart rate. Maturational changes in heart rate variability (HRV) were also documented. Low-frequency (LF: 0.25-0.8 Hz) power of HRV is a marker of both sympathetic and parasympathetic influences. and high-frequency (HF: 0.8-2.4 Hz) power is a marker of efferent vagal activity. Total power (TP) is the sum of LF and HF. TP, normalized units of LF (LF as percent of TP), and normalized HF power decreased from D1 to D7 in all groups. Cocaine treatment affected both LF and HF powers and there was an interaction between cocaine treatment and age for both LF and HF. Although LF/HF ratio decreased from D1 to D7 in both groups of control animals. LF/HF did not change from D1 to D7 in either cocaine-treated group. Thus, cocaine exposure significantly attenuated the age-dependent change in LF/HF. Our results indicated that there were normal developmental changes in HRV consistent with continued postnatal development of autonomic nervous system. Perinatal cocaine exposure appeared to modify these changes. The specific autonomic mechanism for the cocaine effect may be a decline in parasympathetic activity and a concomitant change in sympathetic activity.