Spatial Buffering during Slow and Paroxysmal Sleep Oscillations in Cortical Networks of Glial CellsIn Vivo

Abstract

The ability of neuroglia to buffer local increases of extracellular K(+) has been known from in vitro studies. This property may confer on these cells an active role in the modulation and spreading of cortical oscillatory activities. We addressed the question of the spatial buffering in vivo by performing single and double intraglial recordings, together with measures of the extracellular K(+) and Ca(2+) concentrations ([K(+)](out) and [Ca(2+)](out)) in the cerebral cortex of cats under ketamine and xylazine anesthesia during patterns of slow sleep oscillations and spike-wave seizures. In addition, we estimated the fluctuations of intraglial K(+) concentrations ([K(+)](in)). Measurements obtained during the slow oscillation indicated that glial cells phasically take up part of the extracellular K(+) extruded by neurons during the depolarizing phase of the slow oscillation. During this condition, the redistribution of K(+) appeared to be local. Large steady increases of [K(+)](out) and phasic potassium accumulations were measured during spike-wave seizures. In this condition, [K(+)](in) rose before [K(+)](out) if the glial cells were located at some distance from the epileptic focus, suggesting faster K(+) diffusion through the interglial syncytium. The simultaneously recorded [Ca(2+)](out) dropped steadily during the seizures to levels incompatible with efficient synaptic transmission, but also displayed periodic oscillations, in phase with the intraseizure spike-wave complexes. In view of this fact, and considering the capability of K(+) to modulate neuronal excitability both at the presynaptic and postsynaptic levels, we suggest that the K(+) long-range spatial buffering operated by glia is a parallel synchronizing and/or spreading mechanism during paroxysmal oscillations.

Cortical Inhibition during Burst Suppression Induced with Isoflurane Anesthesia

“…Both results are surprising findings especially since isoflurane is frequently used for the treatment of status epilepticus at concentrations which induce BS (Kofke et al, 1985(Kofke et al, , 1989Meeke et al, 1989). This therapeutic effect probably relies on the ability of isoflurane to block gap junctions (Mantz et al, 1993), a primary instrument in the generalization of spike-wave seizures (Amzica et al, 2002). The above described paradox underlines the complexity, and probably the heterogeneity, of the epileptic syndromes.…”

Mechanisms of physiological and epileptic HFO generation

“…Later on, this rhythmic GABAergic inhibition progressively decreases driven by the collapse of chloride gradients together with a desychronization of interneuronal firing (Derchansky et al, 2008;Dzhala et al, 2010;Gnatkovsky et al, 2008;Lasztoczi et al, 2009;Timofeev et al, 2002b;Viitanen et al, 2010). Then, the local EEG is dominated by large changes in extracellular potassium and calcium that contribute to sustained potentials and slow down oscillatory activity (Amzica et al, 2002;Heinemann et al, 1977;Kaila et al, 1997). Thus, the major cellular generators contributing to the broad range of HFO could evolve dynamically as a seizure progresses and cannot be ascribed to a unique source.…”

Plasticity of astroglial networks in olfactory glomeruli

“…So far, V m fluctuations in astrocytes have mostly been reported from in vivo experiments (16,22) In KO Cx43 mice, dye coupling was diminished by 66% in the presence of TTX when injections were performed in glomerular astrocytes (n = 6 for both control and TTX conditions; P < 0.001), whereas in KO Cx30 animals, dye coupling was not affected by TTX treatment (78% of control, n = 10 and n = 6 for control and TTX conditions, respectively; P = 0.1462). Note that in the control condition, the number of coupled cells was reduced by 42% (n = 6, P < 0.001) and 29% (n = 10, P < 0.001) in KO Cx43 and KO Cx30 mice, respectively, compared with wild type (n = 26).…”