Molecular processes regulating the gain of NMDA receptors modulate diverse physiological and pathological responses in the CNS. Group I metabotropic glutamate receptors (mGluRs), which neighbor NMDA receptors and which can be coactivated by synaptically released glutamate, couple to several different second messenger pathways, each of which could target NMDA receptors. In CA3 pyramidal cells we show that the activation of mGluR1 potentiates NMDA current via a G-protein-independent mechanism involving Src kinase activation. In contrast, mGluR5-mediated enhancement of NMDA current requires G-protein activation, triggering a signaling cascade including protein kinase C and Src. These results indicate that one neurotransmitter, glutamate, can activate two distinct and independent signaling systems to target the same effector. These two pathways are likely to contribute significantly to the highly differentiated control of NMDA receptor function.

We reviewed computer models that have been developed to reproduce and explain epileptiform activity. Unlike other already-published reviews on computer models of epilepsy, the proposed overview starts from the various types of epileptiform activity encountered during both interictal and ictal periods. Computational models proposed so far in the context of partial and generalized epilepsies are classified according to the following taxonomy: neural mass, neural field, detailed network and formal mathematical models. Insights gained about interictal epileptic spikes and high-frequency oscillations, about fast oscillations at seizure onset, about seizure initiation and propagation, about spike-wave discharges and about status epilepticus are described. This review shows the richness and complementarity of the various modeling approaches as well as the fruitful contribution of the computational neuroscience community in the field of epilepsy research. It shows that models have progressively gained acceptance and are now considered as an efficient way of integrating structural, functional and pathophysiological data about neural systems into "coherent and interpretable views". The advantages, limitations and future of modeling approaches are discussed. Perspectives in epilepsy research and clinical epileptology indicate that very promising directions are foreseen, like model-guided experiments or model-guided therapeutic strategy, among others.

For efficient information processing during cognitive activity, functional brain networks have to rapidly and dynamically reorganize on a sub-second time scale. Tracking the spatiotemporal dynamics of large scale networks over this short time duration is a very challenging issue. Here, we tackle this problem by using dense electroencephalography (EEG) recorded during a picture naming task. We found that (i) the picture naming task can be divided into six brain network states (BNSs) characterized by significantly high synchronization of gamma (30-45 Hz) oscillations, (ii) fast transitions occur between these BNSs that last from 30 msec to 160 msec, (iii) based on the state of the art of the picture naming task, we consider that the spatial location of their nodes and edges, as well as the timing of transitions, indicate that each network can be associated with one or several specific function (from visual processing to articulation) and (iv) the comparison with previously-used approach aimed at localizing the sources showed that the network-based approach reveals networks that are more specific to the performed task. We speculate that the persistence of several brain regions in successive BNSs participates to fast and efficient information processing in the brain.