Forskolin modulates acetylcholine release in the hippocampus independently of adenylate cyclase activation
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Published on: June 24, 2015
C Allgaier1, B K Choi, G Hertting
1Institut für Pharmakologie und Toxikologie, Universität Freiburg, F.R.G.
Abstract:
[3H]Acetylcholine release from slices of rabbit hippocampus was elicited by electrical field stimulation (360 pulses/3 Hz). Both forskolin, commonly used as a specific activator of adenylate cyclase, as well as 1,9-dideoxy-forskolin, which fails to activate adenylate cyclase, increased the evoked transmitter release in an almost identical manner. In addition, the phosphodiesterase inhibitor, rolipram, and the membrane-permeable analogue of cAMP, 8-Br-cAMP, did not influence acetylcholine release. These data show that forskolin is not specific to adenylate cyclase and that the increase in acetylcholine release in the rabbit hippocampus occurs through a mechanism other than activation of adenylate cyclase.
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