The involvement of spinal opioid receptors and spinal monoaminergic systems, in the antinociceptive effect of intrathecal (IT) salmon calcitonin, has been evaluated by means of the hot plate test, in the rat. Intrathecal pretreatment with 40 μg MR 1452 and 40 μg ICI 154,129, purported selective antagonists respectively for κ and δ opioid receptors did not modify sCT-induced antinociception (2 μg IT). A delay in the development of IT sCT-induced antinociception was observed in rats selectively depleted of cord serotonin (25 mg/kg IP desipramine plus 100 μg IT 5,7-dihydroxytryptamine), whereas the administration of serotonergic antagonists, methysergide and ketanserin, 30 μg IT, did not influence sCT effect. Cord catecholamine depletion (6-OHDA pretreatment) reduced significantly sCT antinociception. A similar reduction was produced by the dopaminergic antagonist haloperidol (15 μg IT), but not by the α-blocker phentolamine (15 μg IT). Findings of this study rule out an involvement of opioid peptidergic system in sCT-induced increase of hot plate latencies at spinal level; a possible involvement of cord dopaminergic receptors is suggested. © 1985.
Romualdi P, Candeletti S, Spampinato S, Ferri S (1985). Studies on the antinociceptive effect of intrathecal salmon calcitonin. PEPTIDES, 6(3), 273-276 [10.1016/0196-9781(85)90385-7].
Studies on the antinociceptive effect of intrathecal salmon calcitonin
Romualdi P;Candeletti S;Spampinato S;Ferri S
1985
Abstract
The involvement of spinal opioid receptors and spinal monoaminergic systems, in the antinociceptive effect of intrathecal (IT) salmon calcitonin, has been evaluated by means of the hot plate test, in the rat. Intrathecal pretreatment with 40 μg MR 1452 and 40 μg ICI 154,129, purported selective antagonists respectively for κ and δ opioid receptors did not modify sCT-induced antinociception (2 μg IT). A delay in the development of IT sCT-induced antinociception was observed in rats selectively depleted of cord serotonin (25 mg/kg IP desipramine plus 100 μg IT 5,7-dihydroxytryptamine), whereas the administration of serotonergic antagonists, methysergide and ketanserin, 30 μg IT, did not influence sCT effect. Cord catecholamine depletion (6-OHDA pretreatment) reduced significantly sCT antinociception. A similar reduction was produced by the dopaminergic antagonist haloperidol (15 μg IT), but not by the α-blocker phentolamine (15 μg IT). Findings of this study rule out an involvement of opioid peptidergic system in sCT-induced increase of hot plate latencies at spinal level; a possible involvement of cord dopaminergic receptors is suggested. © 1985.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.