Vasodilation evoked from medulla and cerebellum is coupled to bursts of cortical EEG activity in rats

E. V. Golanov, D. J. Reis

Research output: Contribution to journalArticle

33 Scopus citations

Abstract

Cerebral blood flow (rCBF), measured by laser-Doppler flowmetry, spontaneously fluctuates at ~6 events/min in the anesthetized rat. These cerebrovascular waves (CWs) are preceded by simultaneous and synchronous bursts of electrocorticographic activity similar to burst- suppression/spindle-burst electroencephalogram patterns. Identical burst-CW complexes are evoked by single electrical pulses of specific sites in the cerebellar fastigial nucleus or rostral ventrolateral medulla. These consist, sequentially, of a constant initial triphasic (positive-negative-positive) potential reversing polarity in lamina V, variable afterbursts, and transient elevations of rCBF appearing ~1.2 s after burst onset. Evoked bursts are occluded by spontaneous bursts appearing <50 s earlier. Procainization of the cortex reversibly blocks burst-CW complexes. Gradually increasing stimulus frequency proportionally increases the numbers of burst-CW complexes before rCBF rises. We conclude that spontaneous and evoked burst-CW complexes result from excitation of common neurons in lamina V. These intracortical 'vasodilator' neurons are spontaneously excited by thalamocortical afferents generating burst-suppression electroencephalogram (EEG) patterns and excited reflexively by afferent signals from the fastigial nucleus or rostral ventrolateral medulla and couple intrinsic neuronal activity to local vascular mechanisms generating vasodilation.

Original languageEnglish (US)
Pages (from-to)R454-R467
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume268
Issue number2 37-2
DOIs
StatePublished - 1995

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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