g(m1)-ganglioside and Brain-Damage--Chronic

Systemic injections of GM1 gangliosides can enhance behavioral recovery from brain damage as measured by a number of cognitive tasks. The functional recovery is not due to GM1-induced alterations in activity, emotional arousal, or heightened sensitivity to mild, noxious stimulation. In addition, the recovery endures long after all treatments are terminated. Although the specific actions by which GM1 treatments facilitate recovery are unknown, evidence does suggest that both anomalous sprouting and protection of neurons from secondary consequences of injury may be involved in the repair process.

Topics: Animals; Avoidance Learning; Brain Damage, Chronic; Brain Injuries; Caudate Nucleus; Escape Reaction; G(M1) Ganglioside; Rats; Reinforcement, Psychology

Aircrews operating at high G forces and altitudes may be exposed to both physiological and physical stresses capable of inducing brain hypoxia. A potential therapeutic tool for the treatment of flight personnel, monosialoganglioside (GM1) has been found to reduce deficits and enhance repair following CNS injury. A survey of experimental evidence concerning the effects of GM1 in the acute phase of CNS injury supports its proposed application for aerospace medicine.

Topics: Animals; Brain Damage, Chronic; G(M1) Ganglioside; Gravitation; Humans; Hypoxia, Brain; Nerve Regeneration; Space Flight

The effects of GM1 monosialoganglioside pretreatment on brain damage resulting from soman-induced seizure activity were examined in this study. Male Sprague-Dawley rats were infused with GM1 via an osmotic minipump connected through a permanent cannula implanted intracerebroventricularly and challenged with soman (83 micrograms/kg, i.e., 1.25 x LD50) 4 d after initiation of GM1 infusion. Electrocorticographic recordings were monitored via indwelling cortical electrodes. Twenty-seven hours after soman administration, anesthetized rats were euthanized via transcardial perfusion with buffered paraformaldehyde. Brains were processed for hematoxylin and eosin (H&E), cresyl violet (CV), and acetylcholinesterase (AChE) histochemistry, and glial fibrillary acidic protein (GFAP) and microtubule-associated protein 2 (MAP2) immunohistochemistry. All soman-challenged rats not infused with GM1 (n = 14) developed status epilepticus (SE).

Topics: Acetylcholinesterase; Animals; Brain; Brain Chemistry; Brain Damage, Chronic; Cholinesterase Inhibitors; Convulsants; Electroencephalography; G(M1) Ganglioside; Glial Fibrillary Acidic Protein; Image Processing, Computer-Assisted; Injections, Intraventricular; Male; Microtubule-Associated Proteins; Nerve Tissue Proteins; Neuroprotective Agents; Neurotoxins; Rats; Rats, Sprague-Dawley; Seizures; Soman; Status Epilepticus

Systemic administration of monosialoganglioside GM1 is efficacious in reducing excitatory amino acid (EAA)-related neurotoxicity in vivo following intracerebroventricular injection of N-methyl-D-aspartate (NMDA) in 7-day-old rats. Five days later, NMDA-treated animals showed extensive brain damage which was accompanied by significant decreases in brain weight, choline acetyltransferase activity and 3H-ouabain binding. All these neurotoxic effects were significantly reduced with ganglioside treatment. Since excessive activation of EAAS is implicated in hypoxic-ischemic brain damage, these results favor the hypothesis that a similar effect is involved in the ability of ganglioside to ameliorate outcome following cerebral ischemia.

Topics: Animals; Brain; Brain Damage, Chronic; Brain Ischemia; Choline O-Acetyltransferase; G(M1) Ganglioside; Injections, Intraventricular; N-Methylaspartate; Organ Size; Ouabain; Rats

After receiving a nigrostriatal hemitransection in the left hemisphere and an electrolytic caudate nucleus (CN) lesion in the right hemisphere, rats were given intraperitoneal injections of saline or GM1-gangliosides. Significantly smaller areas of terminal degeneration were seen in the substantia nigra pars reticulata (SNr) ipsilateral to the caudate lesion of animals treated with GM1. No statistical differences were seen in the number of degenerating terminals in the CN and SNr on the side with the hemitransection. Exogenous GM1 may thus be effective in preventing anterograde degeneration following brain injury.

Topics: Animals; Basal Ganglia Diseases; Brain Damage, Chronic; Caudate Nucleus; Corpus Striatum; G(M1) Ganglioside; Male; Neural Pathways; Rats; Rats, Inbred Strains; Substantia Nigra

The purpose of the present study was to assess the effects of ganglioside treatment on changes in emotional, activity, and avoidance behaviors following septal brain damage. Rats were treated with GM1-gangliosides either before and after septal lesions, or only after septal lesions and tested for emotionality on 10 consecutive days beginning on the second day after surgery. The ganglioside treatment decreased the emotionality of rats with septal damage on the first test day, and enhanced their rate of recovery to control levels of emotionality. Septal rats treated with gangliosides had activity, rearing, and avoidance behaviors equivalent to nontreated septal rats; however, lesioned rats treated with GM1 showed reduced intertrial crossings during avoidance conditioning. These results suggest that the changes in emotional behavior of septal rats treated with GM1 occur shortly after the lesion.

Topics: Animals; Brain Damage, Chronic; Emotions; G(M1) Ganglioside; Male; Neurocognitive Disorders; Rats; Rats, Inbred Strains; Septum Pellucidum

An increasing focus on the mechanism of synaptic neurochemistry in pediatric neurology, may lead to a better understanding of the pathophysiology of many disorders and result in a more rational approach to their pharmacotherapy. With the burgeoning list of putative neurotransmitters in brain, and the growing evidence of co-localization of many of these neurotransmitters, chemical neurotransmission likely involves a higher degree of complexity than appreciated heretofore. The potential role of neurotransmitter dysfunction in the pathophysiology of neurologic and behavior disorders of children, should not be considered as restricted to those disorders that involve selective neuronal loss, but may encompass a much wider spectrum of syndromes due to metabolic abnormalities, as well as disturbances of the finer features of chemical neurotransmission.

Topics: Afferent Pathways; Animals; Brain Damage, Chronic; Cats; Central Nervous System; Cerebral Cortex; Chemical Phenomena; Chemistry; Child; Child, Preschool; G(M1) Ganglioside; gamma-Aminobutyric Acid; Gangliosidoses; Humans; Mental Disorders; Methylazoxymethanol Acetate; Nerve Tissue; Nervous System Diseases; Neurons; Neurotransmitter Agents; Rats; Sympathetic Nervous System; Synapses; Tourette Syndrome