We investigated the properties of action potential after-potentials in cultured dorsal root ganglion neurones from neonatal rats using the whole cell patch clamp technique. The aims of this study were to characterize after-potentials and investigate the possible influences of Ca2+-induced Ca2+release (CICR) on neuronal excitability. The reversal potentials of action potential after-depolarizations and after-hyperpolarizations were estimated. Although evidence for both Ca2+-activated chloride and potassium conductances was obtained, the data indicated that the after-potentials were contaminatied by a variety of distinct ionic events. Apamin was used to attenuate potassium conductances and appeared to enhance the after-depolarizations due to Ca2+-activated chloride conductances. Ba2+ substitution for Ca2+ significantly broadened the duration of evoked action potentials, which were followed by large-amplitude after-depolarizations. The chloride channel blocker niflumic acid was used to identify Ca2+-activated chloride conductances. Studies were also carried out with ryanodine to investigate divalent cation-induced -Ca2+ release. However, ryanodine attenuated both the prolonged Ba2+-action potentials and after-depolarizations. We conclude that cultured DRG neurones express a variety of channels, which can contribute to action potential after-potentials and thus provide distinct and variable influences on neuronal excitability.

We investigated the properties of action potential after-potentials in cultured dorsal root ganglion neurones from neonatal rats using the whole cell patch clamp technique. The aims of this study were to characterize after-potentials and investigate the possible influences of Ca2+-induced Ca2+release (CICR) on neuronal excitability. The reversal potentials of action potential after-depolarizations and after-hyperpolarizations were estimated. Although evidence for both Ca2+-activated chloride and potassium conductances was obtained, the data indicated that the after-potentials were contaminatied by a variety of distinct ionic events. Apamin was used to attenuate potassium conductances and appeared to enhance the after-depolarizations due to Ca2+-activated chloride conductances. Ba2+ substitution for Ca2+ significantly broadened the duration of evoked action potentials, which were followed by large-amplitude after-depolarizations. The chloride channel blocker niflumic acid was used to identify Ca2+-activated chloride conductances. Studies were also carried out with ryanodine to investigate divalent cation-induced -Ca2+ release. However, ryanodine attenuated both the prolonged Ba2+-action potentials and after-depolarizations. We conclude that cultured DRG neurones express a variety of channels, which can contribute to action potential after-potentials and thus provide distinct and variable influences on neuronal excitability.