4‐Aminopyridine‐induced increase in basal and stimulation‐evoked [
We have examined the mechanisms by which the K+‐channel blocker 4‐aminopyridine (4‐AP) can dose‐dependently increase both basal [3H]‐noradrenaline ([3H]‐NA) release and the [3H]‐NA release evoked by electrical stimulation, but not the release of [3H]‐acetylcholine ([3H]‐ACh), from slices of rat hippocampus.
Both the electrically evoked and the 4‐AP‐induced release were blocked by tetrodotoxin (TTX) (3 μ
The 4‐AP‐induced release could be inhibited by CdCl2(10 μ
Transmitter release evoked by 100 μ
The results suggest that 4‐AP can depolarize some nerve endings in the central nervous system, leading to transmitter release that is dependent on nerve impulses and Ca2+. Furthermore, the fact that α2‐receptors and adenosine A1 receptor agonists can influence the release of NA evoked by 4‐AP suggests that these drugs may have actions that are independent of blockade of aminopyridine‐sensitive K+‐channels.
Document Type: Research Article
Affiliations: Department of Pharmacology, Karolinska Institutet, Box 60 400, S-104 01 Stockholm, Sweden
Publication date: March 1, 1991