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Summary This paper presents a new methodology to obtain the line impedance of current railway tracks by using only short-circuit measurements. Open-circuit measurements required by conventional methodologies are discarded, since they cannot be carried out for railway tracks in service (electrically continuous and indefinite length). The mathematical basis of the proposed methodology is based on the transmission line theory but focused on the changes in track length. The proposal has been successfully applied to characterize the impedance of the high-speed railway line at the Spanish AVE Madrid–Valencia (Cuenca) and in the AVE Atocha–Chamartin tunnel (Madrid). Copyright © 2014 John Wiley & Sons, Ltd.

Mutations in phosphatase and tensin homolog deleted on chromosome 10 (PTEN) are implicated in neuropsychiatric disorders including autism. Previous studies report that PTEN knockdown in neurons in vivo leads to increased spine density and synaptic activity. To better characterize synaptic changes in neurons lacking PTEN, we examined the effects of shRNA knockdown of PTEN in basolateral amygdala neurons on synaptic spine density and morphology by using fluorescent dye confocal imaging. Contrary to previous studies in the dentate gyrus, we find that knockdown of PTEN in basolateral amygdala leads to a significant decrease in total spine density in distal dendrites. Curiously, this decreased spine density is associated with increased miniature excitatory postsynaptic current frequency and amplitude, suggesting an increase in number and function of mature spines. These seemingly contradictory findings were reconciled by spine morphology analysis demonstrating increased mushroom spine density and size with correspondingly decreased thin protrusion density at more distal segments. The same analysis of PTEN conditional deletion in the dentate gyrus demonstrated that loss of PTEN does not significantly alter total density of dendritic protrusions in the dentate gyrus, but does decrease thin protrusion density and increases density of more mature mushroom spines. These findings suggest that, contrary to previous reports, PTEN knockdown may not induce de novo spinogenesis, but instead may increase synaptic activity by inducing morphological and functional maturation of spines. Furthermore, behavioral analysis of basolateral amygdala PTEN knockdown suggests that these changes limited only to the basolateral amygdala complex may not be sufficient to induce increased anxiety-related behaviors.

Sleep-wake behavior is tightly controlled in many animal species, suggesting genetically encoded, homeostatic control mechanisms that determine arousal-state dynamics. We reported that two voltage-gated potassium channels, Kv3.1 and Kv3.3, control sleep in wild-type and Kv3-mutant mice. Compared with wild-type (WT), homozygous double mutants (DKO) that lack these channels sleep 40% less in the light and 22% less in the dark. To understand how the lack of these channels affects sleep, we analysed arousal-state changes during the light period where the differences are greatest between WT and DKO. We determined the kinetic complexity of each arousal state from the episode durations of wakefulness, slow-wave sleep and rapid eye movement sleep (REMS). Based on the number of exponential components in episode-duration histograms, WT and DKO mice have several kinetically distinct states of wakefulness, and these states are longer in duration in DKO. For slow-wave sleep, WT mice have a single slow-wave sleep (SWS) state in contrast to DKO mice, which show two distinct SWS states, one that is 60% shorter than that in WT and a second that is similar in duration. Both WT and DKO mice have two kinetically distinct REMS states. DKO mice show an 84% reduction in the frequency of short REMS episodes ( 60 s). In contrast to the stochastic control of episode durations of wakefulness and SWS, the durations of both REMS states are normally distributed, indicating that the underlying control processes are fundamentally different.