1. Calcium currents in rabbit area postrema neurons were studied with
the perforated patch-clamp technique. Experimental conditions eliminat
ed Na+ and K+ currents and identified both low- and high-threshold vol
tage-activated calcium currents. 2. Low-threshold, T-type calcium curr
ents 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 inactiva
tion near -95 mV, reached half-maximal inactivation at -71 mV and was
totally inactivated by -40 mV. 3. A high-threshold transient current w
as recorded in all area postrema neurons, which consisted of both a tr
ansient and sustained component. This current was present at voltages
greater than -40 mV and the transient component of this current was re
sponsible for the majority of the total Ca2+ current. 4. Nickel ions (
10 mu M) effectively reduced both the T-type current and the high-thre
shold current. Cadmium ions (100 mu M) effectively reduced the high-th
reshold current while having insignificant effects on the low-threshol
d current. 5. Application of the dihydropyridine antagonist nimodipine
(1-10 mu M) had no effect on either the low- or high-threshold voltag
e-activated calcium Ca2+ in area postrema neurons. In addition, applic
ation of omega-conotoxin-GVIA (2-10 mu M) was also without effect on e
ither the low- or high-threshold voltage-activated Ca2+ current, sugge
sting that area postrema neurons possess neither L- or N-type voltage-
activated Ca2+ currents. 6. Application of omega-conotoxin MVIIC (10 m
u M) significantly inhibited the peak high-threshold Ca2+ current by 6
5.4% suggesting that area postrema neurons do possess a omega-conotoxi
n MVIIC-sensitive high-threshold Ca2+ channel. 7. Arg-vasopressin (150
nM) significantly increased the transient component of the high-thres
hold Ca2+ current but bad little effect on either the low-threshold or
the high-threshold sustained component.