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

In this study we demonstrate that 50 mM K+ stimulates the conversion of L-[3H]arginine to L-[3H]citrulline and that this effect is blocked by 10 microM N omega-nitro-L-arginine, a nitric oxide synthase inhibitor, and Ca(2+)-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 mM Mg2+, 100 microM Cd2+, and 10 mM 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 microM Ni2+, 10 microM nifedipine, and 100 nM omega-conotoxin did not.