Publication Date:
1993-10-29
Description:
There is an increasing amount of experimental evidence that oxidative stress is a causal, or at least an ancillary, factor in the neuropathology of several adult neurodegenerative disorders, as well as in stroke, trauma, and seizures. At the same time, excessive or persistent activation of glutamate-gated ion channels may cause neuronal degeneration in these same conditions. Glutamate and related acidic amino acids are thought to be the major excitatory neurotransmitters in brain and may be utilized by 40 percent of the synapses. Thus, two broad mechanisms--oxidative stress and excessive activation of glutamate receptors--are converging and represent sequential as well as interacting processes that provide a final common pathway for cell vulnerability in the brain. The broad distribution in brain of the processes regulating oxidative stress and mediating glutamatergic neurotransmission may explain the wide range of disorders in which both have been implicated. Yet differential expression of components of the processes in particular neuronal systems may account for selective neurodegeneration in certain disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coyle, J T -- Puttfarcken, P -- New York, N.Y. -- Science. 1993 Oct 29;262(5134):689-95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Harvard Medical School, Belmont, MA 02178.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7901908" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Brain/metabolism
;
Glutamates/*physiology
;
Glutamic Acid
;
Humans
;
Nervous System Diseases/*metabolism
;
Neurotransmitter Agents/*physiology
;
Reactive Oxygen Species/*metabolism
;
Receptors, Glutamate/physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
