142 replies to this topic

[thefirstimmortal]

“Glutamate Neurotoxicity: A Three-Stage Process.” In Neurotoxicity of Excitatoiy Amino Acids, edited by A. Guidotti, (1990): 235-242.

[thefirstimmortal]

Demopoulos, HG., Flamm, E.S., and Seigman, M.L. “Membrane Perturba­tions in Central Nervous System Injury: Theoretical Basis for Free Radical Damage and a Review of the Experimental Data.” In Neural Trauma, edited by A.J. Popp, et al. New York: Raven Press, 1979. Other good reviews included: Imlay, J.A., and Linn, S. “DNA Damage and Oxygen Radical Toxicity.” Sci. 240(1988): 1302-1309; and Schmidley, J.W “Free Radicals in Central Nervous System Ischemia.” Stroke 21(1990):1986-1990.

[thefirstimmortal]

Schanne, F.A., Kane, A.B., et al. “Calcium Dependence of Toxic Cell Death: A Final Common Pathway.” Sci. 206(1979): 700-702.

[thefirstimmortal]

Baethmann, A., Maier-Hauff, K., et al. “Release of Glutamate and of Free Fatty Acids in Vasogenic Brain Edema.” J. Neurosurgery 70 (1989): 578-591. This is an excel­lent paper which demonstrates that not only does glutamate accumulate with brain injury but so does arachidonic acid. In fact, in this study, glutamate accumulated in the area of injury in concentrations 1000 to 1500 times normal. This was not transported from the plasma, but rather was secondary to local release of glutamate from the astro­cytes. Arachidonic acid concentrations were higher than that seen in the plasma.

[thefirstimmortal]

Remember, the release of amchidonic acid is triggered by glutamate. This study demon­strates that acute elevations of glutamate in the brain can result from trauma. Nutrition­ists are now recommending that glutamate and glutamine be added to tube feedings to promote better gut function in the traumatized and severely ill patient. This study should caution against this, especially in the neurosurgical patient, many of whom have impaired blood-brain barrier mechanisms.

[thefirstimmortal]

Theoretical Basis for Free Radical Damage and a Review of Experimental Data.” In Neural Trauma, edited by Popp AJ, et al. New York:Raven Press, 1979.

[thefirstimmortal]

Choi, D.E. “Glutamate Neurotoxicity and Diseases of the Nervous System.” Neuron 1(1988): 623-634. This is an excellent review article which covers all aspects of glutamate toxicity.

[thefirstimmortal]

McDonald, JW. and Johnston, M.V. “Physiological Roles of Excitatory Amino Acids During Central Nervous System Development.” Brain Res. 15(1990): 41-70.

[thefirstimmortal]

Maragos, W.F., Greenamyre, J.T, et al. “Glutamate Dysfunction in Alzheimer s Disease: An Hypothesis.” TINS 10(1987): 65-68.

[thefirstimmortal]

Spencer, P.S., Nunn, P.B., et al. “Guam Amyotrophic Lateral Sclerosis-Parkin­sonism-Dementia Linked to a Plant Toxin Excitant Neurotoxin.” Sci. 237(1987):

[thefirstimmortal]

Plaitakis, A. “Glutamate Dysfunction and Selective Motor Neuron Degeneration in Amyotrophic Lateral Sclerosis: An Hypothesis.” Ann. Neurol. 28(1990): 3-8.

[thefirstimmortal]

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

[thefirstimmortal]

Greenamyre, J.T. and Young, A.B. “Excitatory Amino Acids and Alzheimcr’s Disease.” Neurobiology of Aging 10(1989): 593-602.

[thefirstimmortal]

Novelli, A., Cox, J.A., and Lysko, P.G. “Neurotoxicity at the N-Methyl-D-Aspartate Receptor in Energy-Compromised Neurons. An Hypothesis for Cell Death in Aging and Disease.” Ann. NYAcad. Sci. 568(1989): 225-233.

[thefirstimmortal]

Mayer, M.L., Westbrook, G.L., and Guthrie, PB. “Voltage-Dependent Block by Magnesium of NMDA Responses in Spinal Cord Neurons.” Naturc 309(1984):261 -263. Also see: Choi, D.W. “Glutamate Neurotoxicity and Disease of the Nervous System.” Neuron 1(1988): 623-634; and Olney, JW., Price, M.T., et al. “The Role of Specific Ions in Glutamate Neurotoxicity.” Neurosci. Let. 65(1986): 65-71.

[thefirstimmortal]

Siesjo, BK., Bengtsson, F., et al. “Calcium, Excitotoxins, and Neuronal Death in the Brain.” Ann. NY Acad. Sci. 568(1989): 234-251. The mitochondria also sequesters calcium ions and acts as a storage site. Both systems require energy for their operation.

[thefirstimmortal]

Retz, J.C. and Coyle, JT. “Kainic Acid Lesion of Mouse Striatum: Effects on Energy Metabolites.” Life Sci. 27(1980): 2495-2500. They found that when kainate was injected directly into the rat striatum there was a significant drop in the concentra­tion of phosphocreatine and ATP. Alteration in brain energy levels occurred as early as 30 minutes and were pronounced at 120 minutes. Lactate levels in the striatum were nearly doubled and glucose levels fell nearly fifty percent. 14C]-2-deoxyglucose autoradiography data shows that there is a marked increase in glucose utilization in the striatum, the overlying cortex, and the limbic structures within two hours of kainate

[thefirstimmortal]

Rosenberg, P.A. and Aizenman, E. “Hundred-Fold Increase in Neuronal Vul­nerability to Glutamate Toxicity in Astrocyte-Poor Cultures of Rat Cerebral Cortex.” Neurosci. Let. 103(1989): 162-168.

[thefirstimmortal]

Stegink, et al. “Comparative Metabolism of Glutamate in the Mouse, Monkey and Man.” In Glutamic Acid: Advances in Biochemisty and Physiology, edited by L.J. Filer, Jr., et al. New York:Raven Press, 1979.

[thefirstimmortal]

Broad, W., Wade, N. Betrayers of the Truth: Fraud and Deceit in the Halls of Science. New York:Touchstonc Books, 1982.

[thefirstimmortal]

Mattson, M.P. “Neurotransmitters in the Regulation of Neuronal Cytoarchitec­ture.” Brain Res. Rev. 13(1988): 179-212

[thefirstimmortal]

Neuron-Dendrite Architecture in Vitro by Glutamate and a Protective Effect of GABA Plus Diazepam.” Soc. Neurosci. Abstracts 13(1987): 367.

[thefirstimmortal]

Cotman, C.W “Specificity of Synaptic Growth in Brain: Remodeling Induced by Kainic Acid Lesions.” Progress in Brain Research 51(1979): 203-215.

[thefirstimmortal]

Reinis, S. and Goldman, J.M. The Development of the Brain: Biological and Functional Perspectives, 211-212. Springfield, IL:Thomas Books, 1980.

[thefirstimmortal]

Malenka, RC. and Nicoll, RA. “NMDA-Receptor Dependent Synaptic Plastic­ity: Multiple Forms and Mechanisms.” Trends in Neurosci. 16(1993): 521-526.

[thefirstimmortal]

Garthwaite, J. “Glutamate, Nitric Oxide and Cell Signalling in the Nervous System.” Trends in Neurosci. 14(1991):

[thefirstimmortal]

While this article chiefly concerns itself with the role of nitric oxide as a transmitter substance and a possible second messenger, it also mentions the importance of”activity-dependent” organization of affer­cnt fibers in relationship to their target neurons during nervous system development. These, the author points out, involve appropriately timed signals from postsynaptic neurons to presynaptic elements. Nitric oxide may be a candidate for such a role in development of three-dimensional structures and the conformational creation of ion channels. There is a close association between glutamatcrgic neurons and nitric oxide. It appears that at least some glutamate type neurons stimulate cGMP within the neurons. It is known that in the embryonic rat cerebellum, NMDA receptors mediate “most, if not all of the cGMP responses to maximally effective concentrations of exogenous glutamate.”

Olncy, JW. “Excitotoxic Food Additives: Functional Tcratologlcal Aspects.” Pro­gress in Brain Research 73(1988): 283-294.

[thefirstimmortal]

McDonald, JW. and Johnson, M.V. “Physiological and Pathophysiologlcal Roles of Excitatory Amino Acids During Central Nervous System Development?’ Brain Res. Rev. 15(1990): 41-70.

[thefirstimmortal]

Brody, J.R, et al. “Effect of Micro-Injections of L-Glutamate into the Hypothala­mus on Attack and Flight Behavior in Cats.” Nature 224(1969): 1330.

[thefirstimmortal]

Klingberg, H., Brankack, J., and Klingberg, E “Long-Term Effects on Behavior After Postnatal Treatment with Monosodium L-Glutamate. Biomed. Biochem. ACTA 46(1987): 705-711.