Withdrawal symptoms in morphine-dependent rats intracerebroventricularly injected with ACTH1-24 and with beta-MSH.
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Biomedical subjects
Publications and source records attributed to R Poggioli.
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Rats treated with chloramphenicol from days 7 to 21 of intrauterine life (50 milligrams per kilogram per day, injected subcutaneously into the mothers) or in the first 3 days of extrauterine life (50 to 100 milligrams per kilogram per day) were trained for avoidance conditioning when 60 days old. The acquisition of the avoidance response was impaired to a highly significant degree in all the treated groups.
ACTH1-24 and beta-endorphin simultaneously injected at 5-10 microgram dose into the lateral ventricle, reciprocally suppress most of their respective behavioural effects (stretching-yawning syndrome, sexual excitement and hyperalgesia for ACTH1-24 and catalepsy and analgesia for beta-endorphin). The results obtained support the hypothesis that ACTH1-24 and beta-endorphin might interact antagonistically at CNS level.
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The injection of ACTH 1--24 into the cerebral ventricles in rats markedly reduces the reaction time in the hot-plate test and the nociception threshold in the tail-stimulation test. Morphine antagonizes and naloxone potentiates this hyperalgesic effect of ACTH. It is proposed that ACTH peptides play a physiological role in nociception.
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2,4-Monofurfurylidene-tetra-O-methyl-sorbitol (MSF), which protects rats against a number of hepatotoxins, also reduces the death rate in mice receiving a crude Amanita phalloides powder (APP) by i.p. route, this protective effect being dose- and time-dependent. MSF-pretreatment greatly reduces APP-induced liver damage and blood serum GOT and GPT increase. MSF antagonizes APP more effectively than do mercaptopropionylglycine (MPG) and silymarin. The results are briefly discussed.
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