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Journal of Neuroscience, Vol 12, 425-429, Copyright © 1992 by Society for Neuroscience
Dynorphin increases extracellular levels of excitatory amino acids in the brain through a non-opioid mechanism
AI Faden
Department of Neurology, Georgetown University School of Medicine, Washington, D.C. 20007.
Administration of dynorphin A-(1-17) (Dyn 1-17), through a microdialysis
probe stereotaxically placed into rat hippocampus, caused marked increases
in the extracellular levels of glutamate and aspartate. The degree and
duration of elevation of these excitatory amino acids (EAA) induced by Dyn
1-17 were dose dependent but were not modified by the centrally active
opioid receptor antagonist nalmefene. At comparable doses, Dyn 2-17, which
is inactive at the opioid receptor, produced similar alterations in EAA as
Dyn 1-17, whereas Dyn 1-8 caused significantly smaller changes of
glutamate. Dynorphin and EAAs have each been implicated as
pathophysiological factors in brain or spinal cord injuries, with
dynorphin's actions shown to involve both opioid and non-opioid components.
The present observations indicate a direct potential linkage between
dynorphin and excitotoxin mechanisms of CNS injury and provide further
support for the concept that dynorphin's pathophysiologic effects may
include non-opioid actions of this peptide.
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