1‐Methyl‐4‐Phenylpyridinium Produces Excitotoxic Lesions in Rat Striatum as a Result of Impairment of Oxidative Metabolism

1‐Methyl‐4‐Phenylpyridinium Produces Excitotoxic Lesions in Rat Striatum as a Result of... Abstract: The effects of 1‐methyl‐4‐phenylpyridinium (MPP+) were studied in rat striatum. Using freeze‐clamp, microwave, and water‐suppressed proton chemical shift magnetic resonance imaging techniques, MPP+ resulted in marked increases in lactate and a depletion of ATP for up to 48 h after the injections. MPP+ produced dose‐dependent depletions of dopamine, serotonin, γ‐aminobutyric acid, and substance P that were partially blocked at 1 week by prior decortication or completely blocked by MK‐801 at 24 h. The lesions showed relative sparing of somatostatin‐neuropeptide Y neurons, consistent with N‐methyl‐D‐aspartate (NMDA) excitotoxicity. MPP+ produces impairment of oxidative phosphorylation in vivo, which may result in membrane depolarization with persistent activation of NMDA receptors and excitotoxic neuronal degeneration. An impairment of energy metabolism may therefore underlie slow excitotoxic neuronal death in neurodegenerative diseases. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurochemistry Wiley

1‐Methyl‐4‐Phenylpyridinium Produces Excitotoxic Lesions in Rat Striatum as a Result of Impairment of Oxidative Metabolism

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Publisher
Wiley
Copyright
Copyright © 1992 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0022-3042
eISSN
1471-4159
D.O.I.
10.1111/j.1471-4159.1992.tb10080.x
Publisher site
See Article on Publisher Site

Abstract

Abstract: The effects of 1‐methyl‐4‐phenylpyridinium (MPP+) were studied in rat striatum. Using freeze‐clamp, microwave, and water‐suppressed proton chemical shift magnetic resonance imaging techniques, MPP+ resulted in marked increases in lactate and a depletion of ATP for up to 48 h after the injections. MPP+ produced dose‐dependent depletions of dopamine, serotonin, γ‐aminobutyric acid, and substance P that were partially blocked at 1 week by prior decortication or completely blocked by MK‐801 at 24 h. The lesions showed relative sparing of somatostatin‐neuropeptide Y neurons, consistent with N‐methyl‐D‐aspartate (NMDA) excitotoxicity. MPP+ produces impairment of oxidative phosphorylation in vivo, which may result in membrane depolarization with persistent activation of NMDA receptors and excitotoxic neuronal degeneration. An impairment of energy metabolism may therefore underlie slow excitotoxic neuronal death in neurodegenerative diseases.

Journal

Journal of NeurochemistryWiley

Published: May 1, 1992

References

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