Asymmetrical protection of neostriatal neurons against transient forebrain ischemia by unilateral dopamine depletion

Yubo Ren, Xiaoda Li, Zao C. Xu

Research output: Contribution to journalArticle

29 Scopus citations

Abstract

Neurons in the dorsal neostriatum are highly vulnerable to transient cerebral ischemia. It has been suggested that excessive dopamine release during ischemia may play an important role in the pathogenesis of postischemic cell death in the neostriatum. However, it remains controversial whether depletion of dopamine protects neurons in the neostriatum against ischemic insult. In the present study, transient forebrain ischemia was induced using the four-vessel occlusion method. Ischemic depolarization was used as an indication of completed ischemia. Under our experimental conditions, ischemia that produces ~21 min ischemic depolarization caused more than 90% of cell death in the dorsolateral neostriatum. Using such ischemia as a standard insult, the effect of dopamine depletion on neostriatal neurons after ischemia was investigated. Dopamine depletion was produced by unilateral injection of 6-OHDA into the substantia nigra. No difference was found between the number of surviving neurons in the left and the right neostriatum after depletion of dopamine on the left side. In contrast, surviving neurons dramatically increased in the right neostriatum after depletion of dopamine on the right side. These results clearly demonstrate an asymmetrical protection of neostriatal neurons against ischemia after dopamine depletion. The mechanisms of this asymmetrical protection may clarify dopamine action on neuronai injury following cerebral ischemia.

Original languageEnglish (US)
Pages (from-to)250-257
Number of pages8
JournalExperimental Neurology
Volume146
Issue number1
DOIs
StatePublished - Jul 1997

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience

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