Furthermore, we observed high intraindividual stability of coherence across two consecutive nights suggesting that despite only a modest genetic contribution, sleep EEG coherence is like a trait. Our findings in adolescent humans are in line with earlier findings in animals that show the primordial cerebral map and its connections are plastic and it is through interaction with the environment that the pattern of brain network connectivity is shaped. Therefore, even in twins living together, small differences in the environment may cascade into meaningful differences in brain connectivity.Decreased GABAergic inhibition due to dysfunction of inhibitory interneurons plays an important role in post-traumatic epileptogenesis. Reduced N-current Ca2+ channel function in GABAergic terminals contributes to interneuronal abnormalities and neural circuit hyperexcitability in the partial neocortical isolation (undercut, UC) model of post-traumatic epileptogenesis. Because brain-derived neurotrophic factor (BDNF) supports the development and maintenance of interneurons, we hypothesized that the activation of BDNF tropomyosin kinase B (TrkB) receptors by a small molecule, TrkB partial agonist, PTX BD4-3 (BD), would correct N channel abnormalities and enhance inhibitory synaptic transmission in UC cortex. Immunocytochemistry (ICC) and western blots were used to quantify N- and P/Q-type channels. We recorded evoked (e)IPSCs and responses to N and P/Q channel blockers to determine the effects of BD on channel function. Field potential recordings were used to determine the effects of BD on circuit hyperexcitability. Chronic BD treatment 1) upregulated N and P/Q channel immunoreactivity in GABAergic terminals; 2) increased the effects of N or P/Q channel blockade on evoked inhibitory postsynaptic currents (eIPSCs); 3) increased GABA release probability and the frequency of sIPSCs; and 4) reduced the incidence of epileptiform discharges in UC cortex. The results suggest that chronic TrkB activation is a promising approach for rescuing injury-induced calcium channel abnormalities in inhibitory terminals, thereby improving interneuronal function and suppressing circuit hyperexcitability.Objective To investigate the effects of a replacement diet with Khorasan wheat products in patients with fibromyalgia, in comparison with a similar replacement diet with control products made from organic semi-whole-grain modern wheat. Design Randomized, double-blinded crossover trial. Setting Outpatient clinic. Subjects Twenty subjects (19 female and one male, mean age = 48.9 ± 12.3 years) with fibromyalgia. Methods Participants were randomly assigned to consume either Khorasan or control wheat products (pasta, bread, crackers, biscuits) for eight weeks and then crossed. Validated self-administered questionnaires were collected from each subject at the beginning and end of each intervention period. Results A general linear model for repeated measurement, adjusted for potential confounders, showed that the overall score reported from each questionnaire improved after both intervention and control periods, but the effect was more evident after the intervention with Khorasan. In particular, a statistically significant difference in Widespread Pain Index (WPI) + Severity Scale (SS) and Functional Outcome of Sleep Questionnaire (FOSQ) was observed, which decreased significantly by 21.5% and 11.7% respectively, only after the Khorasan period, while no statistically significant variations were reported after the control period. Similarly, FM Impact Questionnaire scores decreased significantly only after the Khorasan period, with a reduction that was significantly different between the intervention and control periods (-22.5% vs -0.3%, P = 0.037). The improvement was even greater in people with higher symptom severity. Conclusions A dietary intervention with Khorasan wheat products seems to benefit patients with fibromyalgia, especially those with greater symptom severity.The notions of degeneracy and redundancy are important constructs in many areas, ranging from genomics through to network science. Degeneracy finds a powerful role in neuroscience, explaining key aspects of distributed processing and structure-function relationships in the brain. For example, degeneracy accounts for the superadditive effect of lesions on functional deficits in terms of a “many-to-one” structure-function mapping. In this paper, we offer a principled account of degeneracy and redundancy, when function is operationalized in terms of active inference, namely, a formulation of perception and action as belief updating under generative models of the world. In brief, “degeneracy” is quantified by the “entropy” of posterior beliefs about the causes of sensations, while “redundancy” is the “complexity” cost incurred by forming those beliefs. From this perspective, degeneracy and redundancy are complementary Active inference tries to minimize redundancy while maintaining degeneracy. Selleckchem SMI-4a This formulation is substantiated using statistical and mathematical notions of degenerate mappings and statistical efficiency. We then illustrate changes in degeneracy and redundancy during the learning of a word repetition task. Finally, we characterize the effects of lesions-to intrinsic and extrinsic connections-using in silico disconnections. These numerical analyses highlight the fundamental difference between degeneracy and redundancy-and how they score distinct imperatives for perceptual inference and structure learning that are relevant to synthetic and biological intelligence.Study question Does NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome activation within decidualized endometrial stromal cells accompany menstruation and is this reflected systemically? Summary answer Components of the NLRP3 inflammasome immunolocalize to decidualized endometrial stromal cells immediately prior to menstruation, and are activated in an in vitro model of menstruation, as evidenced by downstream interleukin (IL)-1beta and IL-18 release, this being reflected systemically in vivo. What is known already Menstruation is a highly inflammatory event associated with activation of NFκB (nuclear factor kappa-light-chain-enhancer of activated B cells), local release of chemokines and cytokines and inflammatory leukocyte influx. Systemically, chemokines and cytokines fluctuate across the menstrual cycle. Study design, size, duration This study examined the NLRP3 inflammasome and activation of downstream IL-1beta and IL-18 in endometrial tissues from women of known fertility (≥1 previous parous pregnancy) across the menstrual cycle (n ≥ 8 per cycle phase), serum from women during the proliferative, secretory and menstrual phases (≥9 per cycle phase) of the cycle and menstrual fluid collected on Day 2 of menses (n = 18).