Abstract
Prostanoid EP receptor-mediated modulation of noradrenaline release from cultured chick sympathetic neurons was investigated. Transmitter release from dissociated cell cultures of embryonic paravertebral ganglia, loaded with [3H]-noradrenaline, was elicited either by electrical field stimulation (36 pulses/3 Hz) or by elevating the extracellular concentration of K+ (to 30 mM; for 2 min).
Prostaglandin E2 (PGE2; 0.01–3 μM) enhanced electrically evolved [3H]-noradrenaline release in a concentration-dependent manner with a maximal increase by about 50% at 1 μM. Also iloprost (0.1–3 μM) increased transmitter release concentration-dependently, whereas misoprostol (0.1–3 μM) had no effect. Indometacin (10 μM) influenced neither evoked release per se nor the enhancement caused by PGE2. AH6809 (3 μM), a selective EP1 receptor antagonist, blocked the enhancement caused by both PGE2 and iloprost. K+-evoked noradrenaline release, which was virtually insensitive to tetrodotoxin (0.3 μM), was increased by PGE2 to an extent comparable to that observed after electrical stimulation.
In summary, the present data indicate that PGE2 facilitates noradrenaline release from cultured chick sympathetic neurons by a receptor which shows the pharmacological profile of the EP1 subtype and is probably located at the processes of the neuron.
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Allgaier, C., Meder, W. Cultured chick sympathetic neurons: prostanoid EP1 receptor-mediated facilitation of noradrenaline release. Naunyn-Schmiedeberg's Arch Pharmacol 352, 447–450 (1995). https://doi.org/10.1007/BF00172784
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DOI: https://doi.org/10.1007/BF00172784