Abstract

In this study we have characterized the functional expression of T-type Ca(2+) channels in developing chick nodose neurons, a population of placode-derived sensory neurons innervating the heart and various visceral organs. Voltage-gated Ca(2+) currents were measured using whole cell patch clamp recordings in neurons acutely isolated between embryonic day (E) 7 and E20, prior to hatching. E7 nodose neurons express relatively large high voltage-activated (HVA) Ca(2+) currents. HVA current density progressively increases between E7 and E17. T-type Ca(2+) currents were restricted to a few nodose neurons between E7 and E10 but were present in approximately 60% of nodose neurons by E17. T-type Ca(2+) channels regulate the response of nodose neurons to injection of hyperpolarizing currents, but do not have any effect on the action potential waveform. Nickel ions blocked T-type Ca(2+) currents in a concentration-dependent manner with an IC(50) of 17 microM. The high sensitivity of T-type Ca(2+) channels to nickel blockade combined with sequencing of a partial cDNA suggests that T-type Ca(2+) currents are generated by alpha1H subunits in chick nodose neurons. Steady-state activation and inactivation kinetics were similar to those previously reported for other alpha1H channels in mammalian neurons. Semi-quantitative PCR analysis indicates that alpha1H mRNA was present in chick nodose neurons by E7, suggesting that the functional expression of T-type Ca(2+) channels involves a posttranscriptional mechanism. These findings demonstrate a distinct pattern of T-type Ca(2+) channel functional expression in placode-derived neurons when compared with CNS neurons.

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