These findings suggest a favourable effect of implicit regulation on instructed fear, which is subserved by less involvement of control-related brain mechanisms. Copyright © 2020 Zhang, Chen, Deng, Yang and Yuan.Spike and wave discharges (SWDs) are a characteristic manifestation of childhood absence epilepsy (CAE). It has long been believed that they unpredictably emerge from otherwise almost normal interictal EEG. Herein, we demonstrate that pretreatment closed-eyes theta and beta EEG wavelet powers of CAE patients (20 girls and 10 boys, mean age 7.4 ± 1.9 years) are much higher than those of age-matched healthy controls at multiple sites of the 10-20 system. For example, at the C4 site, we observed a 100 and 63% increase in power of theta and beta rhythms, respectively. We were able to compare the baseline and posttreatment wavelet power in 16 patients. Pharmacotherapy brought about a statistically significant decrease in delta and theta wavelet power in all the channels, e.g., for C4 the reduction was equal to 45% (delta) and 63% (theta). The less pronounced attenuation of posttreatment beta waves was observed in 13 channels (36% at C4 site). The beta and theta wavelet power were positively correlated with the percentage of time in seizure (defined as the ratio of the duration of all absences which patients experienced to the duration of recording) for majority of channels. We hypothesize that the increased theta and beta powers result from cortical hyperexcitability and propensity for epileptic spike generation, respectively. We argue that the distinct features of CAE wavelet power spectrum may be used to define an EEG biomarker which could be used for diagnosis and monitoring of patients. Copyright © 2020 Glaba, Latka, Krause, Kuryło, Jernajczyk, Walas and West.Homer proteins are a component of the post-synaptic density of neurons that are necessary for the maintenance and consolidation of behavioral state. The dominant negative protein homer1a is rapidly increased by neuronal activity and sleep loss. Homer1a knockout mice with globally absent homer1a have reduced ability to sustain wakefulness during the active period. It is not known whether homer1a is required globally or in very specific brain regions or neurons for its role in maintaining wake. In this study, we examined the expression of homer1a, an immediate early gene involved in intracellular signaling cascades, in mice subjected to extended wakefulness. We found that mice displayed increased expression of homer1a in the claustrum, a brain region thought to be involved in consciousness, as well as the cingulate and piriform cortices compared to non-sleep deprived mice. In situ hybridization (ISH) studies also indicate that homer1a is not induced in the known wake promoting regions with sleep deprivation, but is instead upregulated primarily in the claustrum and piriform cortex. Examination of homer1a expression levels with recovery sleep after sleep deprivation indicate that baseline homer1a expression levels were restored. Further, we have identified that homer1a is upregulated in excitatory neurons of the claustrum suggesting that homer1a promotes wakefulness through activating excitatory neurons. This work identifies regions previously unknown to be involved in sleep regulation that respond to acute sleep deprivation or enhanced waking. Copyright © 2020 Zhu, Hafycz, Keenan, Guo, Pack and Naidoo.Spiking neural networks (SNNs) present a promising computing model and enable bio-plausible information processing and event-driven based ultra-low power neuromorphic hardware. However, training SNNs to reach the same performances of conventional deep artificial neural networks (ANNs), particularly with error backpropagation (BP) algorithms, poses a significant challenge due to inherent complex dynamics and non-differentiable spike activities of spiking neurons. In this paper, we present the first study on realizing competitive spike-train level backpropagation (BP) like algorithms to enable on-chip training of SNNs. We propose a novel spike-train level direct feedback alignment (ST-DFA) algorithm, which is much more bio-plausible and hardware friendly than BP. Algorithm and hardware co-optimization and efficient online neural signal computation are explored for on-chip implementation of ST-DFA. On the Xilinx ZC706 FPGA board, the proposed hardware-efficient ST-DFA shows excellent performance vs. overhead tradeoffs for real-world speech and image classification applications. SNN neural processors with on-chip ST-DFA training show competitive classification accuracy of 96.27% for the MNIST dataset with 4× input resolution reduction and 84.88% for the challenging 16-speaker TI46 speech corpus, respectively. Compared to the hardware implementation of the state-of-the-art BP algorithm HM2-BP, the design of the proposed ST-DFA reduces functional resources by 76.7% and backward training latency by 31.6% while gracefully trading off classification performance. Copyright © 2020 Lee, Zhang, Zhang, Liu and Li.Fear memory generalization is a learning mechanism that promotes flexible fear responses to novel situations. While fear generalization has adaptive value, overgeneralization of fear memory is a characteristic feature of the pathology of anxiety disorders. The neuropeptide S (NPS) receptor (NPSR) has been shown to be associated with anxiety disorders and has recently been identified as a promising target for treating anxiety disorders. Moreover, stress hormones play a role in regulating both physiological and pathological fear memories and might therefore also be involved in anxiety disorders. However, little is known about the interplay between stress hormone and the NPS system in the development of overgeneralized fear. Here, we hypothesize that NPSR-deficient mice with high corticosterone (CORT) levels during the fear memories consolidation are more prone to develop generalized fear. https://www.selleckchem.com/products/hrs-4642.html To address this hypothesis, NPSR-deficient mice were submitted to a contextual fear conditioning procedure. Immediately after conditioning, mice received CORT injections (2.5 or 5 mg/kg). One day and 1 month later, the mice were tested for the specificity and strength of their fear memory, their anxiety level, and their startle response. Moreover, CORT blood levels were monitored throughout the experiment. Using this protocol, a specific contextual fear memory was observed in all experimental groups, despite the 5-mg/kg CORT-treated NPSR-deficient mice. This group of mice showed a generalization of contextual fear memory and a decreased startle response, and the females of this group had significantly less body weight gain. These findings indicate that interplay between CORT and the NPS system during the consolidation of fear memories is critical for the generalization of contextual fear. Copyright © 2020 Kolodziejczyk and Fendt.