1 The e ect of the administration of pertussis toxin (PTX) as well as modulators of di erent subtypes of K+ channels on the antinociception induced by clonidine and guanabenz was evaluated in the mouse hot plate test. 2 Pretreatment with pertussis toxin (0.25 mg per mouse i.c.v.) 7 days before the hot-plate test, prevented the antinociception induced by both clonidine (0.08 ± 0.2 mg kg71, s.c.) and guanabenz (0.1 ± 0.5 mg kg71, s.c.). 3 The administration of the KATP channel openers minoxidil (10 mg per mouse, i.c.v.), pinacidil (25 mg per mouse, i.c.v.) and diazoxide (100 mg kg71, p.o.) potentiated the antinociception produced by clonidine and guanabenz whereas the KATP channel blocker gliquidone (6 mg per mouse, i.c.v.) prevented the a2 adrenoceptor agonist-induced analgesia. 4 Pretreatment with an antisense oligonucleotide (aODN) to mKv1.1, a voltage-gated K+ channel, at the dose of 2.0 nmol per single i.c.v. injection, prevented the antinociception induced by both clonidine and guanabenz in comparison with degenerate oligonucleotide (dODN)-treated mice. 5 The administration of the Ca2+-gated K+ channel blocker apamin (0.5 ± 2.0 ng per mouse, i.c.v.) never modi®ed clonidine and guanabenz analgesia. 6 At the highest e ective doses, none of the drugs used modi®ed animals' gross behaviour nor impaired motor coordination, as revealed by the rota-rod test. 7 The present data demonstrate that both KATP and mKv1.1 K+ channels represent an important step in the transduction mechanism underlying central antinociception induced by activation of a2 adrenoceptors.

Role of potassium channels in the antinociception induced by agonists of alpha2-adrenoceptors / N. GALEOTTI; C. GHELARDINI; M.C.VINCI; A. BARTOLINI. - In: BRITISH JOURNAL OF PHARMACOLOGY. - ISSN 0007-1188. - STAMPA. - 126:(1999), pp. 1214-1220. [10.1038/sj.bjp.0702395]

Role of potassium channels in the antinociception induced by agonists of alpha2-adrenoceptors

GALEOTTI, NICOLETTA;GHELARDINI, CARLA;BARTOLINI, ALESSANDRO
1999

Abstract

1 The e ect of the administration of pertussis toxin (PTX) as well as modulators of di erent subtypes of K+ channels on the antinociception induced by clonidine and guanabenz was evaluated in the mouse hot plate test. 2 Pretreatment with pertussis toxin (0.25 mg per mouse i.c.v.) 7 days before the hot-plate test, prevented the antinociception induced by both clonidine (0.08 ± 0.2 mg kg71, s.c.) and guanabenz (0.1 ± 0.5 mg kg71, s.c.). 3 The administration of the KATP channel openers minoxidil (10 mg per mouse, i.c.v.), pinacidil (25 mg per mouse, i.c.v.) and diazoxide (100 mg kg71, p.o.) potentiated the antinociception produced by clonidine and guanabenz whereas the KATP channel blocker gliquidone (6 mg per mouse, i.c.v.) prevented the a2 adrenoceptor agonist-induced analgesia. 4 Pretreatment with an antisense oligonucleotide (aODN) to mKv1.1, a voltage-gated K+ channel, at the dose of 2.0 nmol per single i.c.v. injection, prevented the antinociception induced by both clonidine and guanabenz in comparison with degenerate oligonucleotide (dODN)-treated mice. 5 The administration of the Ca2+-gated K+ channel blocker apamin (0.5 ± 2.0 ng per mouse, i.c.v.) never modi®ed clonidine and guanabenz analgesia. 6 At the highest e ective doses, none of the drugs used modi®ed animals' gross behaviour nor impaired motor coordination, as revealed by the rota-rod test. 7 The present data demonstrate that both KATP and mKv1.1 K+ channels represent an important step in the transduction mechanism underlying central antinociception induced by activation of a2 adrenoceptors.
1999
126
1214
1220
N. GALEOTTI; C. GHELARDINI; M.C.VINCI; A. BARTOLINI
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Utilizza questo identificatore per citare o creare un link a questa risorsa: https://hdl.handle.net/2158/307905
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