“…These changes were not seen in the control slices perfused with no-Mg aCSF without drug delivery. Rather, SLE frequency during control recordings tended to increase with time, in keeping with previous studies (Voss et al 2010 ). Fig.…”
The general anesthetic propofol has been in clinical use for more than 30 years and has become the agent of choice for rapid intravenous induction. While its hypnotic and anti-convulsant properties are well known, the propensity for propofol to promote seizure activity is less well characterised. Electroencephalogram-confirmed reports of propofol-induced seizure activity implicate a predisposition in epileptic subjects. The aim of this study was to investigate the seizure-promoting action of propofol in mouse brain slices—with the goal of establishing an in vitro model of propofol pro-convulsant action for future mechanistic studies. Coronal slices were exposed to either normal artificial cerebrospinal fluid (aCSF) or no-magnesium (no-Mg) aCSF—and extracellular field potential recordings made from the hippocampus, entorhinal cortex and neocortex. Propofol (and etomidate for comparison) were delivered at three stepwise concentrations corresponding to clinically relevant levels. The main finding was that propofol induced ictal-like seizures in seven out of ten hippocampal recordings (p = 0.004 compared to controls) following pre-exposure to no-Mg aCSF—but strongly inhibited seizure-like event (SLE) activity in the neocortex. Propofol did not induce seizure activity in slices exposed to normal aCSF. The results support the contention that propofol has the capacity to promote seizure activity, particularly when there is an underlying seizure predisposition. This study establishes an in vitro model for exploring the mechanisms by which propofol promotes subcortical seizure activity.
“…These changes were not seen in the control slices perfused with no-Mg aCSF without drug delivery. Rather, SLE frequency during control recordings tended to increase with time, in keeping with previous studies (Voss et al 2010 ). Fig.…”
The general anesthetic propofol has been in clinical use for more than 30 years and has become the agent of choice for rapid intravenous induction. While its hypnotic and anti-convulsant properties are well known, the propensity for propofol to promote seizure activity is less well characterised. Electroencephalogram-confirmed reports of propofol-induced seizure activity implicate a predisposition in epileptic subjects. The aim of this study was to investigate the seizure-promoting action of propofol in mouse brain slices—with the goal of establishing an in vitro model of propofol pro-convulsant action for future mechanistic studies. Coronal slices were exposed to either normal artificial cerebrospinal fluid (aCSF) or no-magnesium (no-Mg) aCSF—and extracellular field potential recordings made from the hippocampus, entorhinal cortex and neocortex. Propofol (and etomidate for comparison) were delivered at three stepwise concentrations corresponding to clinically relevant levels. The main finding was that propofol induced ictal-like seizures in seven out of ten hippocampal recordings (p = 0.004 compared to controls) following pre-exposure to no-Mg aCSF—but strongly inhibited seizure-like event (SLE) activity in the neocortex. Propofol did not induce seizure activity in slices exposed to normal aCSF. The results support the contention that propofol has the capacity to promote seizure activity, particularly when there is an underlying seizure predisposition. This study establishes an in vitro model for exploring the mechanisms by which propofol promotes subcortical seizure activity.
“…An example of the type of activity recorded is shown in figure 1. While not quantified in this study, the frequency of the seizure-like activity averages approximately one to three events per minute, with each event 2-6 s in length (Voss et al 2010). Cortical slices held in normal ACSF are quiescent and do not exhibit the local-field potential activity.…”
Section: Cortical Slice and Sample Preparationmentioning
confidence: 87%
“…The mice were not genetically modified in any way. Cortical slices were prepared from adult female animals according to standard procedures (Voss et al 2010). The brains were extracted following carbon dioxide anaesthesia and decapitation.…”
Section: Cortical Slice and Sample Preparationmentioning
confidence: 99%
“…In this paper, we have been motivated to explore further the relationship between the three areas of tissue conductivity, gap junction connectivity and seizure. In addition to the computer modelling of Steyn-Ross et al (2007), experimental work by one of us (Voss et al 2010) showed that seizures in slices from mice deficient in Cx-36 gap junctions were less able to be reduced by applying general anaesthetic agents than seizures in slices from wild-type mice, thus suggesting an experimental link between gap junction connectivity and propensity for the seizure. This work helps pull together previous work and these ideas by looking specifically In this paper, we report on measurements of conductivity made in vitro, from sections of both seizing and non-seizing brain slices.…”
The electrical conductivity of small samples of mouse cortex (in vitro) has been measured at 10 kHz through the four-electrode method of van der Pauw. Brain slices from three mice were prepared under seizing and non-seizing conditions by changing the concentration of magnesium in the artificial cerebrospinal fluid used to maintain the tissue. These slices provided 121 square samples of cortical tissue; the conductivity of these samples was measured with an Agilent E4980A four-point impedance monitor. Of these, 73 samples were considered acceptable on the grounds of having good electrical contact between electrodes and tissue excluding outlier measurements. Results show that there is a significant difference (p = 0.03) in the conductivities of the samples under the two conditions. The seizing and non-seizing samples have mean conductivities of 0.33 and 0.36 S m(-1), respectively; however, these quantitative values should be used with caution as they are both subject to similar systematic uncertainties due to non-ideal temperature conditions and non-ideal placement of electrodes. We hypothesize that the difference between them, which is more robust to uncertainty, is due to the changing gap junction connectivity during seizures.
“…Our experiments, in line with others (reviewed in Neuenschwander et al, 2002), provide strong evidence for long-range synchrony in the cat retina. Thus, junctional coupling is likely to be preserved under halothane (or isoflurane), although some evidence shows that GABAergic anesthetics may suppress gap junction function (Voss et al, 2010; Wentlandt et al, 2006).…”
Fast gamma oscillations, generated within the retina, and transmitted to the cortex via the lateral geniculate nucleus (LGN), are thought to carry information about stimulus size and continuity. This hypothesis relies mainly on studies carried out under anesthesia and the extent to which it holds under more naturalistic conditions remains unclear. Using multi-electrode recordings of spiking activity in the retina and the LGN of the cat, we show that visually driven gamma oscillations are absent for awake states and are highly dependent on halothane (or isoflurane). Under ketamine, responses were non-oscillatory, as in the awake condition. Response entrainment to the monitor refresh was commonly observed up to 120 Hz and was superseded by the gamma oscillatory responses induced by halothane. Given that retinal gamma oscillations are contingent upon halothane anesthesia and absent in the awake cat, such oscillations should be considered artifactual, thus playing no functional role in vision.
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