Stimulation of the subthalamic vasodilator area and fastigial nucleus independently protects the brain against focal ischemia. Academic Article uri icon

Overview

abstract

  • We investigated whether stimulation of the functionally discrete subthalamic region, subthalamic cerebrovasodilator area (SVA), which increases cerebral blood flow (CBF) when excited, would, like stimulation of cerebellar fastigial nucleus (FN), produce central neurogenic neuroprotection. A 1-h electrical stimulation of SVA or FN reduced infarctions triggered by permanent occlusion of middle cerebral artery (MCA) by 48-55% in Sprague-Dawley rats and by 59% in Fisher rats. The salvaging effect of SVA stimulation, similar to FN, was long lasting and reduced the volume of infarctions placed 72 h or 10 days later by 58 and 26%, respectively, in Fisher rats. Bilateral lesioning of FN neurons by the microinjection of ibotenic acid 5 days before SVA stimulation did not affect SVA-evoked neuroprotection. Bilateral lesions of SVA neurons administered 5 days before FN stimulation had no effect on FN-induced neuroprotection but reversed the stimulus-locked increase in CBF accompanying FN stimulation. This study demonstrates that (1) excitation of neurons and/or fibers projecting through the SVA reduces ischemic infarctions as substantially as excitation of FN neurons; (2) the effects are long-lasting and not attributable to increases in cerebral blood flow, changes in blood gases or brain temperature, or rat strain; (3) the neuroprotective effects of SVA and FN stimulation are mutually independent and (4) FN-evoked cerebrovasodilation is mediated by SVA neurons. The SVA and FN are part of a neuronal system in CNS, which is distributed and, when excited, acts to protect the brain from ischemic injury.

publication date

  • August 31, 2001

Research

keywords

  • Brain Ischemia
  • Cerebellar Nuclei
  • Cerebrovascular Circulation
  • Electric Stimulation Therapy
  • Nerve Degeneration
  • Subthalamus
  • Vasodilation

Identity

Scopus Document Identifier

  • 0035979859

Digital Object Identifier (DOI)

  • 10.1016/s0006-8993(01)02602-6

PubMed ID

  • 11520492

Additional Document Info

volume

  • 912

issue

  • 1