The reactivity of an electroencephalogram (EEG) to external stimuli is impaired in comatose patients showing burst-suppression (BS) patterns following hypoxic–ischemic brain injury (HIBI). We ...explored the reactivity of BS induced by isoflurane in rat models of HIBI and controls using intermittent photic stimulation (IPS) delivered to one eye. The relative time spent in suppression referred to as the suppression ratio (SR) was measured on the contralateral fronto-occipital cortical EEG channel. The BS reactivity (BSR) was defined as the decrease in the SR during IPS from the baseline before stimulation (SRPRE). We found that BSR increased with SRPRE. To standardize by anesthetic depth, we derived the BSR index (BSRi) as BSR divided by SRPRE. We found that the BSRi was decreased at 3 days after transient global cerebral ischemia in rats, which is a model of brain injury after cardiac arrest. The BSRi was also reduced 2 months after experimental perinatal asphyxia in rats, a model of birth asphyxia, which is a frequent neonatal complication in humans. Furthermore, Oxytocin attenuated BSRi impairment, consistent with a neuroprotective effect in this model. Our data suggest that the BSRi is a promising translational marker in HIBI which should be considered in future neuroprotection studies.
The role of nonapeptides in the modulation of sleep has been described by several studies; yet, little evidence is found on the effects on sleep of oxytocin (OT), a nonapetide involved in human ...social behaviour and in the regulation of the hypothalamo-pituitary-adrenal axis. The aim of the present study is to examine whether intranasal administration of OT has any effect on sleep architecture. Ten healthy male volunteers were included in a double-blind, cross-over study and were randomly administered nasal instillations of either placebo or OT. A one-month washout period was allowed between the administrations of each substance. Polysomnographic recordings were performed: before the beginning of drug administration, after seven days and after one month. We found that long-term administration of OT influences sleep architecture by reducing sleep latencies, increasing the sleep efficiency and increasing the percent of REM sleep episodes.
Foetal asphyxia, a frequent birth complication, detrimentally impacts the immature brain, resulting in neuronal damage, uncontrolled seizure activity and long-term neurological deficits. Oxytocin, a ...neurohormone mediating important materno-foetal interactions and parturition, has been previously suggested to modulate the immature brain's excitability, playing a neuroprotective role. Our aim was to investigate the effects of exogenous oxytocin administration on seizure burden and acute brain injury in a perinatal model of asphyxia in rats.
Asphyxia was modelled by exposing immature rats to a 90-minute episode of low oxygen (9% O
) and high CO
(20% CO
). Control rats were kept in ambient room-air for the same time interval. In a third group of experiments, oxytocin (0.02 UI/g body weight) was nasally administered 30 minutes before the asphyxia episode. Seizure burden was assessed by the cumulative number of loss of righting reflex (LRR) over a two-hour postexposure period. Acute brain injury was assessed through hippocampal S-100 beta, a biomarker of cellular injury, 24-hours after exposure.
Asphyxia increased both LRR and hippocampal S-100 beta protein compared to controls, and these effects were significantly reduced by oxytocin administration.
Oxytocin treatment decreased both seizure burden and hippocampal injury, supporting a potential neuroprotective role for oxytocin in perinatal asphyxia.
The purpose of this study is to assess the frontal and parietal ECoG spectrum (gamma range) changes during isoflurane and combined xenon-isoflurane anaesthesia in rats.
Experiments were carried out ...on four adult male Sprague-Dawley rats (250-300 g). The anaesthesia was induced with isoflurane and maintained with isoflurane and a xenon-isoflurane mixture. The rats were maintained at two different anaesthetic depths: light (isoflurane anaesthesia) and deep (isoflurane and xenon-isoflurane anaesthesia). The frontal and the parietal cortical activity was assessed by computing the median frequency, spectral edge frequency and functional connectivity between these two areas during light and deep anaesthesia.
We noticed a decrease in cortical connectivity under deep isoflurane anaesthesia and an increase in connectivity under deep xenon-isoflurane anaesthesia. Moreover, during xenon-isoflurane anaesthesia, a trend of regularity of electro-cortical activity was present compared with isoflurane anaesthesia.
Xenon-isoflurane deep anaesthesia demonstrated a series of specific ECoG features regarding frontoparietal functional connectivity (gamma range connectivity increase) and regularity of the electrocortical activity compared with isoflurane anaesthesia.
Global cerebral ischemia induces, within seconds, suppression of spontaneous electrocortical activity, partly due to alterations in synaptic transmission. In vitro studies have found that repeated ...brief hypoxic episodes prolong the persistence of synaptic transmission due to weakened adenosine release. The aim of this study was to investigate in vivo whether the time to ischemic electrocortical suppression (TES) could be altered during energy stress conditions such as rapid repeated global cerebral ischemia and kainate‐induced seizures. Experiments were carried out in adult rats under chloral hydrate anaesthesia. Repeated episodes of 1 min of ischemia were induced by transiently clamping the carotid arteries in a ‘four‐vessel occlusion’ model. We devised an automatic method of TES estimation based on the decay of the root mean square of two‐channel electrocorticographic recordings. To distinguish the alterations in spontaneous electrocortical activity we compared TES with the ischemic suppression of visual evoked potentials (VEP). During the first ischemic episode, TES was ∼ 15 s and remained unchanged when five ischemic episodes were separated by 10‐min reperfusion intervals. When ischemia was repeated after 2 min of reperfusion TES progressively increased, reaching a plateau value of ∼ 24 s. A similar plateau was reached during kainate‐induced seizures. The TES plateau occurred prior to ischemic suppression of VEP. Our data suggest that, under conditions of acute metabolic stress in vivo, the ischemic suppression of spontaneous electrocortical activity may be delayed up to a plateau value. These findings are consistent with the hypothesis of a depletable adenosine pool; however, the restoration of synaptic transmission may be faster in vivo than in vitro.
The aim of this study was to evaluate the frontal intracortical connectivity during deep anaesthesia (burst-suppression).
Experiments were carried out on 5 adult Sprague Dawley rats. The anaesthesia ...was induced and maintained with isoflurane. Following the induction of anaesthesia, rats were placed in a stereotactic instrument. A hole was drilled in the skull over the frontal cortex and electrodes were inserted in order to record the local field potentials. Rats were maintained in deep level anaesthesia (burst-suppression). The cortical connectivity was assessed by computing the coherence spectra. The frontal intracortical connectivity was calculated during burst, suppression (non-burst) and slow wave anaesthesia periods.
The global cortical connectivity (0.5-100 Hz) was 0.61 ± 0.078 during the burst periods compared to 0.55 ± 0.032 (p < 0.05) during the suppression periods and 0.55 ± 0.015 (p < 0.05) during slow wave anaesthesia.
The global cortical connectivity increased during the burst periods compared to the suppression periods and slow wave anaesthesia. This increase in the cortical synchronization might be due to the subcortical origin of the bursts.
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