Turkish Journal of Medical Sciences




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 Ca^{2+}-induced Ca^{2+}release (CICR) on neuronal excitability. The reversal potentials of action potential after-depolarizations and after-hyperpolarizations were estimated. Although evidence for both Ca^{2+}-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 Ca^{2+}-activated chloride conductances. Ba^{2+} substitution for Ca^{2+} 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 Ca^{2+}-activated chloride conductances. Studies were also carried out with ryanodine to investigate divalent cation-induced -Ca2+ release. However, ryanodine attenuated both the prolonged Ba^{2+}-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.


Ryanodine, after-potentials, cultured sensory neurones, apamin and niflumic acid.

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