A mesoscale network model is proposed for the development of spike and wave discharges (SWDs) in the cortico-thalamo-cortical (C-T-C) circuit. It is based on experimental findings in two genetic models of childhood absence epilepsy–rats of WAG/Rij and GAERS strains. The model is organized hierarchically into two levels (brain structures and individual neurons) and composed of compartments for representation of somatosensory cortex, reticular and ventroposteriomedial thalamic nuclei. The cortex and the two thalamic compartments contain excitatory and inhibitory connections between four populations of neurons. Two connected subnetworks both including relevant parts of a C-T-C network responsible for SWD generation are modelled: a smaller subnetwork for the focal area in which the SWD generation can take place, and a larger subnetwork for surrounding areas which can be only passively involved into SWDs, but which is mostly responsible for normal brain activity. This assumption allows modeling of both normal and SWD activity as a dynamical system (no noise is necessary), providing reproducibility of results and allowing future analysis by means of theory of dynamical system theories. The model is able to reproduce most time-frequency changes in EEG activity accompanying the transition from normal to epileptiform activity and back. Three different mechanisms of SWD initiation reported previously in experimental studies were successfully reproduced in the model. The model incorporates also a separate mechanism for the maintenance of SWDs based on coupling analysis from experimental data. Finally, the model reproduces the possibility to stop ongoing SWDs with high frequency electrical stimulation, as described in the literature.

We demonstrate the dissipative spatiotemporal patterns that are generated by an active ring resonator based on a magnonic quasicrystal (MQC) with Fibonacci-type structure. The dissipative patterns are formed through the magnetostatic surface spin-wave (MSSW) parametric decay into exchange spin waves (SWs), temporal dispersion of the ring resonator and amplification. In the spatial domain, the MSSW and SW parametric patterns measured with the help of Brillouin light spectroscopy have the quasiperiodic spatial localization in crests and grooves of the MQC, respectively. In contrast to the optical quasiperiodic parametric spatial conservative solitons, the amplitude profiles of the magnonic quasiperiodic parametric spatial dissipative patterns correspond to the profiles of the crests and grooves of the MQC. In the time domain, the packets of the chaotic parametric pulses, which are analogs of temporal solitons, are generated at each point of the spatial patterns. The chaotic nature of such pulses is confirmed by an estimate of a highest Lyapunov exponent from the experimental time series. The pulse packets are formed through the time-filtering technique using the external microwave (MW) pulses to control a ring gain. It is shown that at a certain duty factor of the external MW pulses, the parametric MSSW pulses have the amplitude and phase profiles corresponding to the profiles of a conservative bright envelope soliton.

In our study, we compare three popular approaches to directed coupling analysis, in particular transfer entropy and two types of Granger causality, applied to real data from genetic absence epilepsy rats. We have chosen the channels for which the coupling architecture is already well known from previous studies. Recordings from 5 WAG/Rij rats of 8 hours duration with at least 28 spontaneous seizures of length not less than 6 s in each recording were studied. To test results for significance, surrogate signals based on series permutation technique were constructed. Connectivity development in time was investigated by considering six two-second intervals before, during and after the seizure. Our outcomes showed large differences between studied approaches, while all of them exploit the same general idea. Transfer entropy demonstrated the smallest number of significant couplings throughout all three considered measures, while the linear Granger causality showed the largest number of them. This indicates that transfer entropy is the most conservative measure and the least sensitive one. Its sensitivity is affected by insufficient series length. The linear Granger causality is likely to demonstrate insufficient specificity.

Spreading depolarization (SD), a self-propagated wave of transient depolarization, regularly occurs in the cortex after acute brain insults and is now referred as an important diagnostic and therapeutic target in patients with acute brain injury. Here, we show that the amygdala, the limbic structure responsible for post-injury neuropsychological symptoms, exhibits strong regional heterogeneity in vulnerability to SD with high susceptibility of its basolateral (BLA) region and resilience of its centromedial (CMA) region to triggering SD by acute focal damage. The BLA micro-injury elicited SD twice as often compared with identical injury of the CMA region (71% vs. 33%). Spatiotemporal features of SDs triggered in the amygdala indicated diverse patterns of the SD propagation to the cortex. Our results suggest that even relatively small cerebral structures can exhibit regional gradients in their susceptibility to SD and the heterogeneity may contribute to the generation of complex SD patterns in the injured brain.