1. We have characterized the actions of arachidonic acid (AA) on whole cell
and unitary calcium (Ca2+) currents in rat neonatal superior cervical gang
lion (SCG) neurons using barium (Ba2+) as the charge carrier.
2. Whole cell currents were elicited by stepping the membrane potential fro
m -90 mV to +10 mV. Arachidonic acid (5 mu M) was introduced into the bath
in the continued presence of 1 mu M (+)-202-791, an L-type Ca2+ channel ago
nist. Under these conditions, the peak current, comprised mainly of N-type
current, and a slow, (+)-202-791-induced component of the tail current were
inhibited by 67 +/- 6 and 60 +/- 10%, respectively, indicating that AA inh
ibits both N- and L-type currents.
3. At a test potential of +30 mV, AA (5 mu M) decreased unitary L- and N-ty
pe Ca2+ channel open probability (P-o) in cell-attached patches that contai
ned a single channel. Fbr both channels, the underlying causes of the decre
ase in P-o were similar. Arachidonic acid caused an increase in the percent
age of null sweeps and in the number of null sweeps that clustered together
. In sweeps with activity, the average number of openings per sweep decreas
ed, while first latency and mean closed time increased. Arachidonic acid ha
d no significant effect on unitary current amplitude or mean open time.
4. Our findings are the first description of the inhibition of unitary L- a
nd N-type Ca2+ channel activity by AA and are consistent with both channels
spending more time in their null mode and with increased dwell time in one
or more closed states.