Behavioral recovery following kainic acid lesions and fetal implants of the striatum occurs independent of dopaminergic mechanisms.

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  • Author(s): Deckel AW; Moran TH; Robinson RG
  • Source:
    Brain research [Brain Res] 1986 Jan 22; Vol. 363 (2), pp. 383-5.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Elsevier/North-Holland Biomedical Press Country of Publication: Netherlands NLM ID: 0045503 Publication Model: Print Cited Medium: Print ISSN: 0006-8993 (Print) Linking ISSN: 00068993 NLM ISO Abbreviation: Brain Res Subsets: MEDLINE
    • Publication Information:
      Original Publication: Amsterdam Elsevier/North-Holland Biomedical Press.
    • Subject Terms:
      Corpus Striatum/*transplantation ; Dopamine/*physiology ; Movement Disorders/*therapy; Animals ; Brain Diseases/chemically induced ; Brain Diseases/therapy ; Corpus Striatum/metabolism ; Female ; Fetus ; Kainic Acid ; Rats ; Rats, Inbred Strains ; Receptors, Dopamine/metabolism ; Synaptic Transmission
    • Abstract:
      Transplantation of fetal striatal tissue into rats with kainic acid lesions of the striatum reversed the spontaneous locomotor abnormalities caused by the lesions, but had no effect on the lesion-induced hyperactivity that followed amphetamine or apomorphine injection. Conversely, transplants into intact (non-lesioned) striatum led to abnormalities in spontaneous locomotion, but did not effect locomotion under amphetamine or apomorphine conditions. Dopamine autoradiography found a relative absence of dopamine receptors within the transplants. These results suggest that the mechanism which accounts for transplant-induced recovery of spontaneous locomotion is independent of striatal dopamine mechanisms.
    • Grant Information:
      RR5378 United States RR NCRR NIH HHS
    • Accession Number:
      0 (Receptors, Dopamine)
      SIV03811UC (Kainic Acid)
      VTD58H1Z2X (Dopamine)
    • Publication Date:
      Date Created: 19860122 Date Completed: 19860324 Latest Revision: 20190614
    • Publication Date:
      20240829
    • Accession Number:
      10.1016/0006-8993(86)91028-0
    • Accession Number:
      3002559