The differential effect of halothane and isoflurane on electroencephalogrphic responses to electrical microstimulation of the reticular formation

Mashawn Orth, Emigdio Bravo, Linda S Barter, Earl Carstens, Joseph F. Antognini

Research output: Contribution to journalArticle

22 Scopus citations


Isoflurane and halothane cause electroencephalographic (EEG) depression and neuronal depression in the reticular formation, a site critical to consciousness. We hypothesized that isoflurane, more than halothane, would depress EEG activation elicited by electrical microstimulation of the reticular formation. Rats were anesthetized with either halothane or isoflurane and stimulating electrodes were positioned in the reticular formation. In a crossover design, anesthetic concentration was adjusted to 0.8 and 1.2 minimum alveolar concentration (MAC) of halothane or isoflurane and electrical microstimulation was performed and the EEG responses were recorded. Microstimulation increased the spectral edge and median edge frequencies 2-2.5 Hz at 0.8 MAC for halothane and isoflurane and 1.2 MAC halothane. At 1.2 MAC isoflurane, burst suppression occurred and microstimulation decreased the period of isoelectricity (24% ± 19% to 8% ± 7%; P < 0.05), whereas the spectral edge and median edge frequencies were unchanged. At anesthetic concentrations required to produce immobility, the cortex remains responsive to electrical microstimulation of the reticular formation, although the EEG response is depressed in the transition from 0.8 to 1.2 MAC. These data indicate that cortical neurons remain responsive to synaptic input during isoflurane and halothane anesthesia.

Original languageEnglish (US)
Pages (from-to)1709-1714
Number of pages6
JournalAnesthesia and Analgesia
Issue number6
StatePublished - Jun 2006


ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

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