g(m1)-ganglioside and Learning-Disabilities

Injections of GM1-gangliosides (30 mg/kg, i.p.) in adult rats were shown to reduce behavioral deficits after brain lesions. This was observed (1) after bilateral electrolytic lesions of the caudate nucleus in a learning task involving negative reinforcement; (2) following aspiration lesions of the mediofrontal cortex in a learning task involving positive reinforcement; and (3) when rotational behavior was assessed after amphetamine or apomorphine injections in animals with partial hemitransections of the nigro-striato-nigral fibers. A detailed anatomical analysis of the latter study, using a retrograde tract-tracing dye wheat germ agglutinin-horseradish peroxidase (WGA-HRP), provided evidence for ganglioside-stimulated, neuronal reorganization of connections to the caudate nucleus. Our findings support the notion that gangliosides reduce behavioral deficits following brain injury by preventing secondary neuronal degeneration and/or enhancing structural reorganization of remaining afferents, rather than by influencing denervation supersensitivity.

Topics: Animals; Brain Injuries; Caudate Nucleus; Corpus Striatum; Frontal Lobe; G(M1) Ganglioside; Gangliosides; Humans; Learning Disabilities; Male; Movement Disorders; Neural Pathways; Rats; Substantia Nigra