142 replies to this topic

[thefirstimmortal]

Olncy, JW., et al. “Glutamate-Induced Brain Damage in Infant Primates.”j Neuropath. &Exp. Neur 31(1972): 464-487.

[thefirstimmortal]

It should be noted that brain concussion is associated with the accumulation of glutamate within the brain, especially in the area of the hippocampus. The source of this glutamate is the brain itself called cndogenous glutamate. It is thought that the high levels of glutamate produce the damage that eventually leads to the “punch drunk” syndrome.

[thefirstimmortal]

Price, B.H., Daffncr, K.R., et al. “The Compartmental Learning Disabilities of Early Frontal Lobe Damage.” Brain 113(1990): 1383-1393.

[thefirstimmortal]

Kerr, G.R., Waisman, H.A. “Transplacental Ratios of Serum-Free Amino Acids During Pregnancy in the Rhesus Monkey.” In Amino Acid Metabolism and Genetic Variation, edited by ‘ML. Nathal, 429-437. New York:McGraw Hill, 1967.

[thefirstimmortal]

Stegnik, L.D., et al. “Placental Transfer of Glutamate and its Mctabolites in the Primate.” Am. J. Obstet. GynecoL 122(1975): 70-78.

[thefirstimmortal]

Kerr, G. R and Waisman, H .A. “Transplacental Ratios of Serum - Free Amino Acids During Pregnancy in the Rhesus Monkey” In Amino Acid Metaholicns and Genetic Variation, edited by ‘ML. Nathal, 429-437. New York:McGraw Hill, 1967.

[thefirstimmortal]

Olney, JW. “Toxic Effects of Glutamate and Related Amino Acids on the Develop­ing Central Nervous System.” In Heritable Disorders ofAmino Acid Metabolism, edited

[thefirstimmortal]

Olney, J.W. “Excitotoxic Food Additives: Functional Teratological Aspects.” In Progress in Brain P..es. Vol. 73, New York:Elscvier Science Publications, 1988.

[thefirstimmortal]

Reinis, S. and Goldman, J.M. “The Development of the Brain” Biological and Functional Perspectives, 211-213. Springfield, IL:Thomas Books, 1980.

[thefirstimmortal]

Olney, J.W. “Glutamate, A Neurotoxic Transmitter.” j Child Neurology 4(1989):218-225

[thefirstimmortal]

. “Eflècts of Neurotoxic Excita­tory Amino Acids on Neuroendocrine Regulation.” In Evcitotoxins, edited by K. Fuxe, et al., 295-305. London:MacMillan Press, 1983.

[thefirstimmortal]

. “Excitotoxic Food Additives: Functional Teratological Aspects.” In Progress in Brain Research Vol. 73, edited by C.J. Boer, et al., 283-294, 1988.

[thefirstimmortal]

Grayson, DR., Szekely, A.M., and Cosa, E. “Glutamate-Induced Gene Expres­sion in Primary Cerebellar Neurons. edited by A. Guidotti New York:Raven Press Ltd., 1990. This gene activation occurs via a second messenger system, inositol triphosphate and diacylglycerol, which have been activated by phospholipase C. Modification of a preexisting transcription factor induces an early response in certain genes.

[thefirstimmortal]

McDonald, J.W and Johnston, M.V. “Physiological and Pathophysiologieal Roles of Excitatory Amino Acids During Central Nervous System Development:’ Brain Bes. Rev. 15(1990): 41-70.

[thefirstimmortal]

Klingberg, H., Brankack, J., et al. “Long-Term Effects on Behavior after Post­natal Treatment with Monosodium L-Glutamate.” Biomed. Biochem. ACTA 26(1987):705-711. In this study they found that in normal rats, early post-natal removal of the eyes caused hyperactivity. MSG treated rats never developed this syndrome but rather had decreased motor activity. The MSG animals behaved like animals with “lowered intelligence

[thefirstimmortal]

l

“Neurotoxicity of Monosodium L-Glutamate in Preg­nant and Fetal Rats.” ACTA Neurapath (Berl) 75(1987): 16-22

[thefirstimmortal]

“Glutamate-Induced Brain Damage in Infant Primates.”j Neumpath. Neur 31 (1972): 464-488. Also of interest is an earlier paper by Dr. Olney in which he found that the excitatory amino acid cysteine could cause widespread damage to the fetal brain, especially in the amygdala, cerebral cortex, hippocampus, and several neuronal groups in the thalamus.

[thefirstimmortal]

Thurston, J.H. and Warren, S.K. “Permeability of the Blood-Brain Barrier to Monosodium Glutamate and Effects on the Components of the Energy Reserve in Newborn Mouse Brains.”j Neumchem. 18 (1971): 2241-2244.

[thefirstimmortal]

Toth, E. and Lajtha, A. “Elevation of Cerebral Levels of Nonessential Amino Acids In Vivo by Administration of Large Doses.” Neumchem. Per. 6(1981): 1309-1317.

[thefirstimmortal]

McDonald, J.W and Johnson, M.V. Brain Research Reviewc 15(1990): 41-70; also, Brewer, G.J. and Cotman, C.W. “NMDA Receptor Regulation of Neuronal Mor­phology in Cultured Hippocampal Neurons.” Neurosci. Let. 99(1989): 268-273; and Mattson, M.P., et al. “Outgrowth-Regulating Actions of Glutamate in Isolated Hip­pocampal Pyramidal Neurons’j Neumsci. 8(1988): 2087-2100.

[thefirstimmortal]

Murphey, T.H., et al. “Immature Cortical Neurons are Uniquely Sensitive to Glutamate Toxicity by Inhibition of Cystine Uptake.” FASEB 6(1990): 1624- 1633.

[thefirstimmortal]

For a more detailed treatment of brain metabolism see: Siesjo, B.K. “Regional Metabolic Rates in the Brain.” In Brain Energy Metabolism, edited by B.K. Seisjo, 131-150. New York:John Wiley & Sons, 1978.

[thefirstimmortal]

Olney, J.W. “Glutamate, A Neurotoxic Transmitter.” j Child Neur 4(1989):218-226. Also see: Rothman, S.M. and Olney, JW “Glutamate and the Pathophysiol­ogy of Hypoxic-Ischemic Brain Damage.” Ann. Neur 19(1986): 105-111; and Kochhar, A., Zivin, J.A., et al. “Glutamate Antagonist Therapy Reduces Neurological Deficits Produced by Focal Central Nervous System Ischemia.” Arch. Neur 45(1988): 148-153. Of particular interest is a study which demonstrated that glutamate and aspartate are increased to very high levels in the extracellular spaces of the brain following global ischemia. This appeared to be time related. After 10 minutes of complete global ische­mia glutamate and aspartate levels increase 4 to 8 fold and by 30 minutes they increased 100 fold. Exogenous glutamate or aspartate could add to this already elevated pool of excitotoxins, especially under conditions of stroke or acute hypertension: conditions where the blood-brain barrier would be broken down.

[thefirstimmortal]

. “Calcium Excitotoxins, and Neuronal Death in the Brain. Ann. NYAcad. Sci. 568(1989): 234-251

[thefirstimmortal]

Chen, M.H., et al. “Ischemic Neuronal Damage after Acute Subdural Hema­toma in the Rat: Effect of Pretreatment with a Glutamate Antagonist.”j Neurosurgery

[thefirstimmortal]

Olney, J.W “Excitotoxins and Neurological Diseases.” Proceedings of the Interna­tional College of Neuropathologist. Kyoto, Japan, 1990.

[thefirstimmortal]

Weiss, J.H. and Choi, D.W. “Differential Vulnerability to Excitatory Amino Acid-Induced Toxicity and Selective Neuronal Loss in Neurodegenerative Diseases.” CanadianJ. Neuroiogical Sci. 18(1991): 394-397.

[thefirstimmortal]

Olney, J.W. “Excitotoxins and Neurological Diseases.” Proceedings of the International College of Neuropath. Kyoto, Japan, 1990. Also see: Olney, J.W “Exeitotoxic Food Additives: Functional Teratological Aspects.” In Progress in Brain Research, edited by, C.J. Boer, et al., Vol. 73, 283-294. New York:Elsevier Science Publications, 1988.

[thefirstimmortal]

Olney, JW. “Brain Lesions, Obesity, and Other Disturbances in Mice Treated with Monosodium Glutamate.” Sci. 165(1969): 719-721.

[thefirstimmortal]

Olney, J.W. “Glutamate-Induced Neuronal Necrosis in the Infimt Mouse Hypo­thalamus. An Electron Microscopic Study.” J. Neuropath. Exp. Neurol. 30(1971):