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. 2014 Apr;349(1):56–65. doi: 10.1124/jpet.113.210708

Fig. 3.

Fig. 3.

Selective PDE4 inhibition with rolipram hyperpolarizes DSM cell resting membrane potential (MP) in a BK channel-dependent manner. (A) An original current-clamp recording illustrating that rolipram (10 µM) hyperpolarized cell MP. The subsequent addition of the BK channel blocker, paxilline (1 µM), inhibited the spontaneous transient hyperpolarizations and depolarized the MP. (B) Summary data illustrating that rolipram (10 µM) hyperpolarized the MP. The subsequent addition of 1 µM paxilline reversed the rolipram-induced hyperpolarization and further depolarized the cell MP back to the control level (n = 8, N = 6; *P < 0.05). (C) An original current-clamp recording illustrating that paxilline (1 µM) abolished the spontaneous transient hyperpolarizations. Rolipram (10 µM) did not exhibit a hyperpolarizing effect on the MP in the presence of 1 µM paxilline. (D) Summary data illustrating that rolipram (10 µM) did not have any effect on the MP in DSM cells pretreated with 1 µM paxilline (n = 7, N = 5; P > 0.05; NS, nonsignificant).