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

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
  • Author(s): Oka T; Hosoya E
  • Source:
    Psychopharmacology [Psychopharmacology (Berl)] 1976 Jun 23; Vol. 47 (3), pp. 243-8.
  • Publication Type:
    Journal Article
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Springer-Verlag Country of Publication: Germany NLM ID: 7608025 Publication Model: Print Cited Medium: Print ISSN: 0033-3158 (Print) Linking ISSN: 00333158 NLM ISO Abbreviation: Psychopharmacology (Berl) Subsets: MEDLINE
    • Publication Information:
      Original Publication: Berlin, New York, Springer-Verlag.
    • Subject Terms:
    • Abstract:
      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.
    • References:
      Eur J Pharmacol. 1973 Apr;22(1):117-9. (PMID: 4706877)
      Life Sci. 1969 May 1;8(9):483-6. (PMID: 5791700)
      Psychopharmacologia. 1963 May 21;4:247-60. (PMID: 14048545)
      Pharmacol Rev. 1966 Jun;18(2):965-96. (PMID: 5328390)
      Eur J Pharmacol. 1969 Aug;7(2):170-5. (PMID: 5345991)
      J Pharmacol Exp Ther. 1966 Dec;154(3):499-516. (PMID: 5297133)
      Pharmacol Rev. 1967 Dec;19(4):463-521. (PMID: 4867058)
      Keio J Med. 1963 Jun;12:83-97. (PMID: 13964155)
      Jpn J Pharmacol. 1970 Sep;20(3):455-7. (PMID: 5312655)
      Psychopharmacologia. 1972;23(3):231-7. (PMID: 5026946)
      Science. 1967 Apr 21;156(3773):402-3. (PMID: 4886538)
      J Pharmacol Exp Ther. 1970 Apr;172(2):406-15. (PMID: 5441162)
      Br J Pharmacol. 1971 Sep;43(1):53-66. (PMID: 5136464)
      Psychopharmacologia. 1970;16(5):369-74. (PMID: 5435873)
    • Accession Number:
      0 (Methyltyrosines)
      0 (Neurotransmitter Agents)
      36B82AMQ7N (Naloxone)
      46627O600J (Levodopa)
      76I7G6D29C (Morphine)
      7C0697DR9I (Atropine)
      C1LJO185Q9 (5-Hydroxytryptophan)
      DL48G20X8X (Scopolamine)
      R5J7E3L9SP (Fenclonine)
    • Publication Date:
      Date Created: 19760623 Date Completed: 19761201 Latest Revision: 20190726
    • Publication Date:
      20231215
    • Accession Number:
      10.1007/BF00427608
    • Accession Number:
      9652