By A. H. Kim, G. A. Kerchner, D. W. Choi (auth.), Dr. Frank W. Marcoux, Dr. Dennis W. Choi (eds.)
"CNS neuroprotection" used to be a typical topic of papers, symposia, and experiences throughout the past "decade of the mind. " certainly, lately, experimental learn of putative neuroprotective brokers triggered scientific trials of diverse drug applicants in acute and persistent human neurodegenerative stipulations. whereas the results of those trials haven't been as winning as at the start was hoping, those have been early explorations, and the pipeline of appropriate rules maintains to develop in energy and intensity. we think that early during this new millennium, crippling issues similar to stroke and Alzheimer's affliction can be taken care of successfully through healing neuroprotective concepts. This quantity of the instruction manual of Experimental Pharmacology titled eNS Neuroprotection offers a pharmacological viewpoint on presently promis ing neuroprotective methods, and a scientific point of view at the demanding situations fascinated about developing the efficacy of those techniques via applicable medical trials. part I, "Mechanistic techniques to CNS Neuroprotection," studies significant damage mechanisms that experience shaped the foundation for lots of prior and current scientific trials carried out world wide. Dr. KIM and associates, Washington college university of drugs, assessment the prestige of blocking off excitotoxicity as an method of CNS neuroprotection. Dr. WANG, Pfizer international study and Development,Ann Arbor Laboratories, outlines facts assisting a contri bution of apoptosis to pathological neuronal or glial phone loss. Drs. BECKER and HALLENBECK, college of Washington and the nationwide Institute on Neuro logical ailments and Stroke, respectively, argue that inhibiting inflammatory pathways within the mind will be neuroprotective. Dr.
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1991). The prominence of this dependence of Ca2+ influx upon Na+ channels in white matter may reflect the absence of glutamate receptor-mediated entry routes available in gray matter. Indeed, in cultured cortical neurons, once NMDA and AMPA receptors are pharmacologically blocked, an additional neuroprotective effect of tetrodotoxin or phenytoin against neuronal death triggered by oxygen-glucose deprivation can be unmasked (LYNCH et al. 1995). These findings suggest that combined therapy targeting both postsynaptic glutamate receptors and axonal Na+ channels may provide more effective neuroprotection than either alone.
Brief glutamate exposure raises intracellular Ca 2+ and destroys these cells even when NMDA receptors are blocked. Ca 2+-permeable AMPA receptors are likely also permeable to Zn 2+ and hence confer vulnerability to Zn 2+neurotoxicity (SENSI et al. 1997; WEISS and SENSI 2000). Besides protecting neuronal subpopulations expressing Ca 2+-permeable AMPA receptors, AMPA antagonists could have value in reducing the excitotoxic loss of oligodendrocytes, which likely also express Ca2+-permeable AMPA receptors (see above).
KIM et al. 2. Glutamate Transport The Ca 2+-dependent, vesicular release of glutamate does not wholly account for the rise in extracellular glutamate concentrations during brain ischemia. A substantial contribution is also made in a Ca2+-independent fashion, by reverse operation of glutamate transporters in both neurons and glia (NICHOLLS and ATTWELL 1990; SZATKOWSKI et al. 1990; ATTWELL et al. 1993; JABAUDON et al. 2000; ROSSI et al. 2000). These transporters normally function to remove glutamate from synapses and thus to terminate a synaptic signaling event.
CNS Neuroprotection by A. H. Kim, G. A. Kerchner, D. W. Choi (auth.), Dr. Frank W. Marcoux, Dr. Dennis W. Choi (eds.)