We present optical observations of SN 2013dx, related to the Fermi burst GRB 130702A, which occurred at red shift z = 0.145. It is the second-best sampled gamma-ray burst (GRB)/supernova (SN) after SN 1998bw. The observational light curves contain more than 280 data points in the uBgrRiz filters until 88 d after the burst, and the data were collected from our observational collaboration (Maidanak Observatory, Abastumani Observatory, Crimean Astrophysical Observatory, Mondy Observatory, National Observatory of Turkey and Observatorio del Roque de los Muchachos) and from the literature. We model numerically the multicolour light curves using the one-dimensional radiation hydrodynamical code stella, previously widely implemented for modelling typical non-GRB SNe. The best-fitting model has the following parameters: pre-SN star mass M = 25 M_⊙; mass of the compact remnant M_CR = 6 M_⊙; total energy of the outburst E_oburst = 3.5 × 10⁵² erg; pre-supernova star radius R = 100 R_⊙; |$M_{\rm ^{56}Ni} = 0.2 \,\rm M_{\odot }$|⁠, which is totally mixed through the ejecta; M_O = 16.6 M_⊙; M_Si = 1.2 M_⊙ and M_Fe = 1.2 M_⊙, and the radiative efficiency of the SN is 0.1 per cent.

Intracerebroventricular (ICV) administration of ouabain, an inhibitor of the Na, K-ATPase, is an approach used to study the physiological functions of the Na, K-ATPase and cardiotonic steroids in the central nervous system, known to cause mania-like hyperactivity in rats. We describe a mouse model of ouabain-induced mania-like behavior. ICV administration of 0.5 µl of 50 µM (25 pmol, 14.6 ng) ouabain into each lateral brain ventricle results in increased locomotor activity, stereotypical behavior, and decreased anxiety level an hour at minimum. Fast-scan cyclic voltammetry showed that administration of 50 µM ouabain causes a drastic drop in dopamine uptake rate, confirmed by elevated concentrations of dopamine metabolites detected in the striatum 1 h after administration. Ouabain administration also caused activation of Akt, deactivation of GSK3β and activation of ERK1/2 in the striatum of ouabain-treated mice. All of the abovementioned effects are attenuated by haloperidol (70 µg/kg intraperitoneally). Observed effects were not associated with neurotoxicity, since no dystrophic neuron changes in brain structures were demonstrated by histological analysis. This newly developed mouse model of ouabain-induced mania-like behavior could provide a perspective tool for studying the interactions between the Na,K-ATPase and the dopaminergic system.

Gap junctions (GJs) are intercellular junctions that allow the direct transfer of ions and small molecules between neighboring cells, and GJs between astrocytes play an important role in the development of various pathologies of the brain, including regulation of the pathological neuronal synchronization underlying epileptic seizures. Recently, we found that a pathological change is observed in astrocytes during the ictal and interictal phases of 4-aminopyridin (4-AP)-elicited epileptic activity in vitro, which was correlated with neuronal synchronization and extracellular epileptic electrical activity. This finding raises the question: Does this signal depend on GJs between astrocytes? In this study we investigated the effect of the GJ blocker, carbenoxolone (CBX), on epileptic activity in vitro and in vivo. Based on the results obtained, we came to the conclusion that the astrocytic syncytium formed by GJ-associated astrocytes, which is responsible for the regulation of potassium, affects the formation of epileptic activity in astrocytes in vitro and epileptic seizure onset. This effect is probably an important, but not the only, mechanism by which CBX suppresses epileptic activity. It is likely that the mechanisms of selective inhibition of GJs between astrocytes will show important translational benefits in anti-epileptic therapies.