To study the possible mechanism(s) underlying unresponsiveness following neocortical seizures, we recorded excitatory postsynaptic potentials (EPSPs) of cortical neurons evoked by ipsilateral cortical stimulation before and after spontaneous or elicited seizures. Regular-spiking neurons (n = 32) were intracellularly recorded in association area five of cats under ketamine-xylazine or barbiturate anesthesia. Compared with control responses, cortically

The cortically generated slow oscillation consists of long-lasting hyperpolarizations associated with depth-positive electroencephalogram (EEG) waves and neuronal depolarizations accompanied by firing during the depth-negative EEG waves. It has previously been shown that, during the prolonged hyperpolarizations, the transfer of information from prethalamic pathways to neocortex is impaired, whereas the intracortical dialogue is maintained. To study

Cerebral ischemia induces a rapid suppression of spontaneous brain rhythms prior to major alterations in ionic homeostasis. It was found in vitro during ischemia that the rapidly formed adenosine, resulting from the intracellular breakdown of ATP, may inhibit synaptic transmission via the A(1) receptor subtype. The link between endogenous A(1) receptor activation during ischemia and the suppression of spontaneous electrocortical activity has not

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 (T(ES)) could be altered during energy stress

We investigated the dependency of electrical seizures produced by cortical undercut upon behavioral states of vigilance in chronically implanted cats. Experiments were performed 1-12 weeks after white matter transection. Multisite field potentials and intracellular activity were recorded from suprasylvian and marginal gyri. Paroxysmal activity developed within days and consisted of spike-wave complexes at 3-4 Hz occurring during the waking state

Cortical injury may lead to clinical seizures. We investigated the changing patterns of the sleep-like slow oscillation and its tendency to develop into paroxysmal activity consisting of spike-wave (SW) complexes at 2-4 Hz following partial deafferentation of the suprasylvian gyrus. Experiments were carried out in anesthetized cats, at different time-intervals (week 1 to week 5, W1-W5) after cortical undercut. Multi-site field potentials and single

This study aims at understanding complex interactions between cortical neurons, glia and blood supply developing during the transition from slow-wave sleep to wakefulness. In spite of essential advances from in vitro and culture preparations, the basic mechanisms of glial interactions with their cellular and ionic environment had remained uninvestigated in vivo. Here we approach this issue by performing simultaneous intracellular recordings of cortical

We studied the mechanisms underlying CO2-dependent DC potential shifts, using epicranial, epidural, epicortical, intraventricular and intraparenchymal (intraneuronal, intraglial and field) recordings in ketamine-xylazine anesthetized cats. DC shifts were elicited by changes in artificial ventilation, causing end tidal CO2 variations within a 2-5% range. Hypercapnia was consistently associated with negative scalp DC shifts (average shift -284.4 micro

Intrinsic properties of thalamic neurons are influenced by synaptic activities in ascending pathways and corticofugal projections as well as by the actions of neurotransmitters released by generalised modulatory systems. We focused on effects of corticothalamic projections on the hyperpolarisation-activated cation current Ih. Intracellular recordings of thalamocortical neurons in the dorsal lateral geniculate (dLG) nucleus were performed in cats

In the first seconds following the onset of the global cerebral ischemia, EEG signal amplitude drops towards a “flat-line” level. This occurs too quickly to be explained only by diffuse unspecific alterations of the cerebral metabolism. The present study investigates the evolution of the ischemic electrocortical suppression along five transient global cerebral ischemia episodes of 1 min duration in rats. One experimental group (N=5) was given