Involvement of Calcium Channels in Depolarization‐Evoked Release of Adenosine from Spinal Cord Synaptosomes

Abstract: The potential involvement of L‐ and N‐type voltage‐sensitive calcium (Ca²⁺) channels and a voltage‐independent receptor‐operated Ca²⁺ channel in the release of adenosine from dorsal spinal cord synaptosomes induced by depolarization with K⁺ and capsaicin was examined. Bay K 8644 (10 nM) augmented release of adenosine in the presence of a partial depolarization with K⁺ (addition of 6 mM) but not capsaicin (1 and 10 μM). This augmentation was dose dependent from 1 to 10 nM and was followed by inhibition of release from 30 to 100 nM. Nifedipine and nitrendipine inhibited the augmenting effect of Bay K 8644 in a dose‐dependent manner, but neither antagonist had any effect on release of adenosine produced by K⁺ (24 mM) or capsaicin (1 and 10 μM) ω‐Conotoxin inhibited K⁺‐evoked release of adenosine in a dose‐dependent manner but had no effect on capsaicin‐evoked release. Ruthenium red blocked capsaicin‐induced release of adenosine but had no effect on K⁺‐evoked release. Although L‐type voltage‐sensitive Ca²⁺ channels can modulate release of adenosine when synaptosomes are partially depolarized with K⁺, N‐type voltage‐sensitive Ca²⁺ channels are primarily involved in K⁺‐evoked release of adenosine. Capsaicin‐evoked release of adenosine does not involve either L‐ or N‐type Ca²⁺ channels, but is dependent on a mechanism that is sensitive to ruthenium red.