1. Calcium currents in rabbit area postrema neurons were studied with the perforated patch-clamp technique. Experimental conditions eliminated Na+ and K+ currents and identified both low and high-threshold voltage- activated calcium currents. 2. Low-threshold, T-type calcium currents were observed in 64% of the area postrema neurons recorded. This current activated near -60 mV and had an average peak amplitude of -36.2 ± 5 pA (mean ± SE) at -40 mV. This current began rapid inactivation near -95 mV, reached half-maximal inactivation at -71 mV and was totally inactivated by - 40 mV. 3. A high-threshold transient current was recorded in all area postrema neurons, which consisted of both a transient and sustained component. This current was present at voltages greater than -40 mV and the transient component of this current was responsible for the majority of the total Ca2+ current. 4. Nickel ions (10 μM) effectively reduced both the T-type current and the high-threshold current. Cadmium ions (100 μM) effectively reduced the high-threshold current while having insignificant effects on the low threshold current. 5. Application of the dihydropyridine antagonist nimodipine (1-10 μM) had no effect on either the low- or high- threshold voltage-activated calcium Ca2+ in area postrema neurons. In addition, application of ω-conotoxin-GVIA (2-10 μM) was also without effect on either the low or high-threshold voltage-activated Ca2+ current, suggesting that area postrema neurons possess neither L- or N-type voltage- activated Ca2+ currents. 6. Application of ω-conotoxin MVIIC (10 μM) significantly inhibited the peak high-threshold Ca2+ current by 65.4% suggesting that area postrema neurons do possess a ω-conotoxin MVIIC sensitive high-threshold Ca2+ channel. 7. Arg vasopressin (150 nM) significantly increased the transient component of the high-threshold Ca2+ current but had little effect on either the low-threshold or the high threshold sustained component.
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