1. The effect of GM1 ganglioside on coerulospinal, noradrenergic, adult neurons and on fetal monoaminergic neurons transplanted into the transected spinal cord of the adult rat.
- Author
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Commissiong JW and Toffano G
- Subjects
- Adrenergic Fibers embryology, Adrenergic Fibers transplantation, Animals, Dopamine physiology, Female, Histocytochemistry, Injections, Nerve Regeneration drug effects, Neurons classification, Neurons embryology, Rats, Rats, Inbred Strains, Spinal Cord cytology, Substantia Nigra cytology, Substantia Nigra embryology, Adrenergic Fibers drug effects, Gangliosides administration & dosage, Graft Survival drug effects, Locus Coeruleus cytology, Neurons drug effects, Spinal Cord drug effects
- Abstract
GM1 ganglioside, thyroxine and hydrocortisone were tested for their ability to improve the survival and growth of fetal locus coeruleus noradrenergic neurons in the transected, adult spinal cord. GM1 alone was also tested for its effect on fetal mesencephalic dopaminergic neurons implanted into a small dorsolateral cavity at the L2 region of the cord previously transected at the T9-T10 region. None of the substances tested had any measurable effect on either of the fetal implants. However, in the GM1- and thyroxine-treated animals the somatic dendrites of the axotomized, noradrenergic, coerulospinal neurons appeared more robust, and more intensely fluorescent, compared to their appropriate controls. GM1 also caused a pronounced sprouting of the axotomized monoaminergic (catecholaminergic and serotonergic) fibres in the rostral region of the cord adjacent to the transection site. All of the mesencephalic dopaminergic implants survived in both the GM1-treated animals and their saline-injected controls. However, their development was apparently not influenced by GM1. The results indicate that GM1 and thyroxine can enhance those aspects of the reactive mechanisms of mature, axotomized, noradrenergic coerulospinal neurons that promote their regeneration. As such, GM1 could become a useful tool in current attempts to foster the regeneration of damaged monoaminergic neurons in the mammalian CNS.
- Published
- 1986
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