Chronic heart failure (CHF) is characterized by decreased cardiac parasympathetic and increased cardiac sympathetic nerve activity. This autonomic imbalance increases the risk of arrhythmias and sudden death in the patients with CHF. We hypothesized that the molecular and cellular alterations of cardiac postganglionic parasympathetic (CPP) neurons located in the intracardiac ganglia (ICG) and sympathetic (CPS) neurons existed in the stellate ganglia (SG) possibly link to the cardiac autonomic imbalance in CHF. Rat CHF was induced by left coronary artery ligation. Single cell real-time PCR and immunofluorescent data showed that L (Ca_v1.2 and Ca_v1.3), P/Q (Ca_v 2.1), N (Ca_v 2.2), and R (Ca_v 2.3) types of Ca⁺⁺ channels were expressed in the CPP and CPS neurons, but CHF only decreased the mRNA and protein expression of N-type Ca⁺⁺ channels in the CPP neurons and did not affect the mRNA and protein expression of all Ca⁺⁺ channel subtypes in the CPS neurons. Patch clamp recording confirmed that CHF reduced N-type Ca⁺⁺ currents and cell excitability in the CPP neurons and enhanced N-type Ca⁺⁺ currents and cell excitability in the CPS neurons. N-type Ca++ channel blocker (1 µM -conotoxin GVIA) lowered Ca⁺⁺ currents and cell excitability in the CPP and CPS neurons from sham and CHF rats. These results suggest that CHF reduces the N-type Ca⁺⁺ channel currents and cell excitability in the CPP neurons and enhances the N-type Ca⁺⁺ currents and cell excitability in the CPS neurons, which may contribute to the cardiac autonomic imbalance in CHF.