The Differential Effects of Halothane and Isoflurane on Electroencephalographic Responses to Electrical Microstimulation of the Reticular Formation

Abstract

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.

Brainstem Stimulation Increases Functional Connectivity of Basal Forebrain-Paralimbic Network in Isoflurane-Anesthetized Rats

“…It could be hypothesized that if FC is indeed essential for brain function and even consciousness, then either spontaneous or exogenously generated increases in the tone of the AAS should augment or reorganize the connectivity patterns in relevant functional networks of the brain (Brown et al, 2011;Lee and Dan, 2012;Mashour et al, 2005). This would be particularly expected in sedated or lightly anesthetized states in which cortical response to an increase in AAS activation is plausible (Orth et al, 2006).…”

Comparative effects of halothane, isoflurane, sevoflurane and desflurane on the electroencephalogram of the rat

“…The BSR increased with increasing concentration of sevoflurane and desflurane, whereas the BSR was almost 100%, at all concentrations of isoflurane, indicating that there was profound cortical depression at the lowest concentration of isoflurane studied (1.25% MAC). Previous studies have compared the EEG effects of halothane with other inhalational agents, particularly isoflurane, and found halothane caused less EEG suppression than isoflurane at equipotent concentrations (Ono et al 1997, Johnson and Taylor 1998, Antunes et al 2003, Orth et al 2006. The MAC of an anaesthetic agent is related to the ability of that agent to prevent response to a noxious stimulus.…”

Multiple Modes of Synaptic Excitation of Olfactory Bulb Granule Cells

“…Another prediction of our model is that interventions that boost overall activity levels in piriform cortex (e.g., focal stimulation or pharmacological disinhibition) should potentiate lateral dendrodendritic inhibition in the olfactory bulb and increase the dissimilarity between activity patterns of evoked by different odorants. At the other extreme, very little local processing may occur in the olfactory bulb when piriform cortex activity is depressed after anesthesia (Destexhe et al, 2003;Orth et al, 2006). The depression of cortical feedback to the bulb may contribute to the coordinate increase in odorevoked mitral cell responsiveness and decrease in response sparseness observed in anesthetized mice in vivo (Rinberg et al, 2006).…”