Rapid Communication: The Role of P‐Type Calcium Channels in the Depolarization‐Induced Activation of Nitric Oxide Synthase in Frontal Cortex

Abstract: In this study we demonstrate that 50 mRS K⁺ stimulates the conversion of L‐[³H] arginine to L‐[³H] citrulline and that this effect is blocked by 10 μM AT‐nitro‐l‐arginine, a nitric oxide synthase inhibitor, and Ca²⁺‐free conditions. Amiloride (1 mM) and low Na⁺ conditions were used to test the possible involvement of the Na⁺‐Ca²⁺ exchanger. These treatments were without effect. The calcium channel blockers 10 mRS Mg²⁺, 100 μM Cd²⁺, and 10 mRS Co²⁺ also blocked the K⁺ response, suggesting the involvement of voltage‐dependent calcium channels (VDCCs). The specific VDCC involved seems to be the P type, as funnel‐web spider toxin blocked the response whereas 200 μMNi²⁺, 10 μM nifedipine, and 100 nMω‐conotoxin did not.