In this study, we have investigated the release of immunoreactive interleukin-1β (irIL-1β) from the rat hypothalamus in vitro. It was found that (1) tissue explants release sizable amounts of irIL-1β (ranging from 0.43 to 0.52 pg/mg of wet tissue) in 20 min incubations; (2) basal release is significantly increased by depolarization induced with 56 mM KCl; (3) K+-induced irIL-1β release is inhibited by the specific blocker of N-type calcium channels, ω-conotoxin, and by verapamil, but not by nifedipine; (4) K+-induced release is also inhibited by the Na+ channel blockers tetrodotoxin and lidocaine; (5) irIL-1β release is significantly increased by noradrenalin; such increase is antagonized by verapamil and the β-blocker propranolol, but not by the α-blocker phentolamine. The present evidence suggests that irIL-1β released by rat hypothalamic explants following KCl depolarization is neuronal in origin.
Tringali, G., Mancuso, C., Mirtella, A., Pozzoli, G., Parente, L., Preziosi, P., Navarra, P., Evidence for the neuronal origin of immunoreactive interleukin-1 beta released by rat hypothalamic explants, <<NEUROSCIENCE LETTERS>>, 1997; (219 (3)3): 143-146. [doi:10.1016/s0304-3940(96)13195-5] [https://hdl.handle.net/10807/344999]
Evidence for the neuronal origin of immunoreactive interleukin-1 beta released by rat hypothalamic explants
Tringali, Giuseppe;Mancuso, Cesare;Pozzoli, Giacomo;Preziosi, Paolo;Navarra, Pierluigi
1996
Abstract
In this study, we have investigated the release of immunoreactive interleukin-1β (irIL-1β) from the rat hypothalamus in vitro. It was found that (1) tissue explants release sizable amounts of irIL-1β (ranging from 0.43 to 0.52 pg/mg of wet tissue) in 20 min incubations; (2) basal release is significantly increased by depolarization induced with 56 mM KCl; (3) K+-induced irIL-1β release is inhibited by the specific blocker of N-type calcium channels, ω-conotoxin, and by verapamil, but not by nifedipine; (4) K+-induced release is also inhibited by the Na+ channel blockers tetrodotoxin and lidocaine; (5) irIL-1β release is significantly increased by noradrenalin; such increase is antagonized by verapamil and the β-blocker propranolol, but not by the α-blocker phentolamine. The present evidence suggests that irIL-1β released by rat hypothalamic explants following KCl depolarization is neuronal in origin.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.



