Effects of humoral modulators and naloxone on morphine-induced changes in the spontaneous locomotor activity of the rat

The s.c. administration of 20 mg/kg of morphine-HCl produced a decrease in the spontaneous locomotor activity (SLMA) of rats. The decrease in SLMA was significantly antagonized by p-chlorophenylalanine (p-CPA). When rats pretreated with p-CPA were given 5-hydroxytryptophan before morphine injection,...

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Bibliographic Details
Published in:Psychopharmacology 1976-01, Vol.47 (3), p.243-248
Main Authors: Oka, T, Hosoya, E
Format: Article
Language:English
Subjects:
5-Hydroxytryptophan - pharmacology
Animals
Atropine - pharmacology
Fenclonine - pharmacology
Levodopa - pharmacology
Male
Methyltyrosines - pharmacology
Morphine - pharmacology
Motor Activity - drug effects
Motor Activity - physiology
Naloxone - pharmacology
Neurotransmitter Agents - physiology
Rats
Scopolamine - pharmacology
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Summary:The s.c. administration of 20 mg/kg of morphine-HCl produced a decrease in the spontaneous locomotor activity (SLMA) of rats. The decrease in SLMA was significantly antagonized by p-chlorophenylalanine (p-CPA). When rats pretreated with p-CPA were given 5-hydroxytryptophan before morphine injection, the marked sedative response to morphine was restored, suggesting that the morphine-induced decrease in SLMA of rats may depend on the release of 5-hydroxytryptamine by morphine. By contrast, the s.c. administration of 5 mg/kg of morphine-HCl produced a significant increase in SLMA of rats. The magnitude of the increase was reduced by atropine, scopolamine or alpha-methyl-p-tyrosine. It appears that both adrenergic and cholinergic mechanisms participate in the increase in SLMA of rats induced by morphine. Both the increase in SLMA produced by 5 mg/kg of morphine and the decrease in SLMA induced by 20 mg/kg of morphine were completely antagonized by the s.c. administration of naloxone-HCl, 0.0625 and 0.25 mg/kg, respectively. Thus, it appears that the receptor with which morphine interacts to produce stimulation is chemically identical with or very similar to the receptor with which morphine combines to induce depression. The former receptors, however, are likely to be located on different neurons from the latter.
ISSN:0033-3158
1432-2072
DOI:10.1007/bf00427608