Em. Pich et al., INVOLVEMENT OF ALPHA-2-RECEPTORS IN THE ANALGESIA INDUCED BY TRANSIENT FOREBRAIN ISCHEMIA IN RATS, Pharmacology, biochemistry and behavior, 45(3), 1993, pp. 607-614
Transient forebrain ischemia induced in rats by the four-vessel occlus
ion method produced analgesic effects in the hotplate test that persis
ted for 2 weeks. Ischemia-induced analgesia was attenuated by low dose
s of alpha2-agonist clonidine (0.01-0.10 mg/kg, IP) and enhanced by lo
w doses of alpha2-antagonists yohimbine (1-2 mg/kg, IP) and idazoxan (
0.25-1.00 mg/kg, IP) administration 7 days after ischemia. Ischemia-in
duced analgesia was not affected by methysergide, naloxone, propranolo
l, or phenoxybenzamine administered 7 days after ischemia, when motor
control and arousal level of rats recovered to normal conditions. The
enhanced response to yohimbine was antagonized by pretreatment with cl
onidine (0.75 mg/kg, IP) and naloxone (10 mg/kg, IP), suggesting the i
nvolvement of endogenous opioid peptides. The enhanced response to yoh
imbine was still present 2 months after ischemia, when preischemic hot
plate threshold was restored. AS alpha2-agonists reduce and alpha2-ant
agonists increase the outflow of central noradrenaline, it is suggeste
d that activation of central noradrenergic systems is involved in the
mediation of ischemia-induced analgesia.