Synchrony Levels During Evoked Seizure-Like Bursts in Mouse Neocortical Slices

Abstract

. Synchrony levels during evoked seizure-like bursts in mouse neocortical slices. J Neurophysiol 90: 1571-1580, 2003; 10.1152/jn.00392.2003. Slices (n ϭ 45) from the somatosensory cortex of mouse (P8-13) generated spontaneous bursts of activity (0.10 Ϯ 0.05 Hz) that were recorded extracellularly. Multiunit action potential (AP) activity was integrated and used as an index of population activity. In this experimental model, seizure-like activity (SLA) was evoked with bicuculline (5-10 M) or N-methyl-D-aspartate (NMDA, 5 M). SLA was an episode with repetitive bursting at a frequency of 0.50 Ϯ 0.06 Hz. To evaluate whether SLA was associated with a change in synchrony, we obtained simultaneous intracellular and extracellular recordings (n ϭ 40) and quantified the relationship between individual cells and the surrounding population of neurons. During the SLA there was an increase in population activity and bursting activity was observed in neurons and areas that were previously silent. We defined synchrony as cellular activity that is consistently locked with the population bursts. Signal-averaging techniques were used to determine this component. To quantitatively assess change in synchronous activity at SLA onset, we estimated the entropy of the single cell's spike trains and subdivided this measure into network burst-related information and noise-related entropy. The burst-related information was not significantly altered at the onset of NMDA-evoked SLA and slightly increased when evoked with bicuculline. The signal-to-noise ratio determined from the entropy estimates showed a significant decrease (instead of an expected increase) during SLA. We conclude that the increased population activity during the SLA is attributed to recruitment of neurons rather than to increased synchrony of each of the individual elements.

Prostaglandin E2-Induced Synaptic Plasticity in Neocortical Networks of Organotypic Slice Cultures

“…Coronal slices of the somatosensory cortex (500 m) were transferred into a recording chamber and submerged under a stream of ACSF (temperature, 30°C; flow rate, 10 ml/min) containing (in mM) 118 NaCl, 3 KCl, 1.5 CaCl 2 , 1 MgSO 4 , 25 NaHCO 3 , 1 NaH 2 PO 4 , and 30 D-glucose equilibrated with carbogen (95% O 2 ; 5% CO 2 ). As described previously (van Drongelen et al, 2003(van Drongelen et al, , 2006, network bursting can be induced in acute isolated neocortical slices from mice by raising potassium concentrations to 5 mM (see Fig. 4).…”

Role of Persistent Sodium Current in Bursting Activity of Mouse Neocortical Networks In Vitro

“…Such neurons could also play a role in triggering ripples that in turn would facilitate seizure generation, not only in the neocortex, but also in the hippocampus (Bragin et al 1999a(Bragin et al ,b,c, 2002Fisher et al 1992;Grenier et al 2001;Traub et al 2001). The cellular bursting property together with a modest level of synchrony and recurrent excitation can lead to a seizurelike pattern (Van Drongelen et al 2003a. Our current result, suggesting that intrinsic cellular bursting properties associated with the Na P current are a critical component of synchronous activity in cortical neuronal populations, agrees well with the reported anticonvulsant action of persistent sodium blockers in some patients with epilepsy (Köhling 2002).…”

“…To obtain stable baseline bursting activity of 0.23 Ϯ 0.08 Hz, 5 mM of [K ϩ ] was used (Van Drongelen et al 2003a). Network activity expressed in bursts per second decreased drastically after adding 20 M riluzole (n ϭ 13) or 50 nM TTX (n ϭ 5) to the bath (Figs.…”

“…In the present study we examined the role of bursting neurons in neocortical networks by selectively blocking persistent sodium (Na P ) currents of pyramidal neurons in brain slices obtained from the neocortex of neonatal mice (P8 -P13), while observing whether this blockade affects the generation of spontaneously generated slow network oscillations (0.1-1 Hz) described previously by Van Drongelen et al (2003a). The spontaneously active isolated neocortical network enabled us to pharmacologically manipulate cellular and network properties, a process that is more difficult under in vivo conditions.…”

The Source of Afterdischarge Activity in Neocortical Tonic–Clonic Epilepsy

“…Epileptiform activity shows a variety of phase transitions: interictal to ictal activity; focal to generalized activity; the tonic to clonic transition; and the spontaneous cessation of epileptiform discharges (Prince et al, 1983;Wong and Prince, 1990;Traub and Miles, 1991;Traub et al, 1993;Dzhala and Staley, 2003;Steriade, 2003;Van Drongelen et al, 2003;Netoff et al, 2004;Pinto et al, 2005). However, the nature of the transitions, although being of obvious importance, remains obscure.…”