Major aspects of neuronal function are regulated by Ca2+ including neurotransmitter release, excitability, developmental plasticity and gene expression.Our previous data demonstrated that sensory neurons isolated from a mouse model with a heterozygous mutation of the neurofibromin Nf1 gene (Nf1+/-) exhibited both greater excitability and release of neuropeptides compared to wild-type mice.To determine the mechanisms of augmented excitability, we found that voltage-dependent sodium currents, but not potassium currents, were enhanced in Nf1+/-neurons.To explore whether voltage-gated calcium currents (ICa) and the contributions of individual Ca2+ channel subtypes to total ICa were altered in Nf1+/-neurons, the totalICa and different subtypes of calcium currents identified by their selective blockers in small diameter DRG neurons isolated from adult wild-type and Nfl+/-mice were recorded using the whole-cell patch clamp technique.Interestingly, although the average peak current densities and the steady-state inactivation properties for ICa were not different, N-type currents were significantly larger in Nf1+/-neurons than in wild-type neurons.Because N-type Ca2+ channels play a critical role in transmitter release, augmentation of channel activity of this subtype may be a key component of the increased neuropeptide release that occurs in Nf1+/-sensory neurons.