Calcium currents and their modulation by strong depolarization in cultured hypertensive and normotensive rat celiac neurons

Abstract

Calcium channels play an important role in decreased neuron spike accommodation in superior cervical ganglia of spontaneously hypertensive rats. We investigated calcium currents in dissociated celiac neurons from normotensive rats and from rats made hypertensive by treatment with Deoxycorticosterone acetate and high salt diet. Both normotensive and hypertensive celiac neurons showed a high-voltage activated calcium current with peak current at −10mv and reversal potential at +45mv. The currents were totally blocked by 200nM cadmium and 30% blocked by 10μM nifedipine. There were no differences in the amplitude and kinetic properties of these calcium currents between normotensive and hypertensive celiac neurons. G-protein inhibitory modulation of calcium channels is critical in the regulation of calcium currents in rat sympathetic neurons. A brief strong depolarization temporarily reverses G-protein inhibition in superior cervical ganglion. We used a +80mv, 200ms depolarization prior to a 0mv voltage step as the strong depolarization. The strong depolarization did not change the amplitude of calcium currents in neurons from either normotensive or hypertensive rats. However, beginning 2s after the application of the strong depolarization, the peak amplitude of the calcium current was decreased by 20% in neurons from hypertensive rats but was not changed in neurons from normotensive rats. This reduction in current amplitude persisted up to 1 minute. These findings show that strong depolarization induces a long-lasting inhibition of calcium current in sympathetic neurons from hypertensive rats.