Neuronal and glial membrane potentials during sleep and paroxysmal oscillations in the neocortex

This study investigated the fluctuations in the membrane potential of corti cal neurons and glial cells during the slow sleep oscillation and spike-wav e (SW) seizures. We performed dual neuron-glia intracellular recordings tog ether with multisite field potential recordings from cortical suprasylvian association areas 5 and 7 of cats under ketamine-xylazine anesthesia. Elect rical stimuli applied to the cortex elicited responses consisting of a biph asic depolarization in glial cells, which was associated with an EPSP-IPSP sequence in neurons. During the slow (<1 Hz) oscillation, extracellular mea surements of the potassium concentration revealed periodic increases with a n amplitude of 1-2 mM, similar in shape to glial activities. We suggest tha t, through their uptake mechanisms, glia cells modulate the neuronal excita bility and contribute to the pacing of the slow oscillation. The slow oscil lation often evolved into SW paroxysms, mimicking sleep-triggered seizures. This transition was associated with increased coupling between the depolar izing events in neurons and glial cells. During seizures, the glial membran e potential displayed phasic negative events related to the onset of the pa roxysmal depolarizing shifts in neurons. These events were not voltage depe ndent and increased their incidence and amplitude with the development of t he seizure. It is suggested that the intraglial transient negativities repr esent field reflections of synchronized neuronal potentials. We propose tha t the mechanisms underlying the neuron-glia communication include, besides the traditional neurotransmitter- and ion-mediated pathways, field effects crossing their membranes as a function of the state of the cortical network .