Kateřina Skálová

Models of maternal immune activation (MIA) often lead to parvalbumin-positive (PV+) interneuron deficits and behavioral alterations resembling autism or schizophrenia. We aimed to characterize the effects of MIA in PV-Cre Long-Evans rats. Pregnant dams received 8 lipopolysaccharide injections (1 mg/kg), on alternating days, starting with gestational day 7. The offspring behavior was tested from postnatal day 5 to adulthood, with tasks assessing motor development, anxiety, exploration, social behavior and sensorimotor gating. Morphological changes in the brain, density of PV+ interneurons and perineuronal nets in the prefrontal cortex, as well as the quantity of PV protein were measured at selected timepoints. We found that MIA in PV-Cre Long-Evans rats failed to elicit the expected schizophrenia- or autism-like deficits. Decrease in PV protein in the prefrontal cortex was present without corresponding decrement of PV+ interneurons, with a paradoxical increase in perineuronal net counts. PV-Cre Long-Evans rat line reacts to the MIA protocol very differently than Wistar rats in previously published studies and is suboptimal for studies of schizophrenia- or autism-like behavioral deficits. Genetic background seems to be an important factor for the outcome in MIA rodent models.

This study investigated whether a single morning session of bright light exposure modulates alertness, cognition, mood, and EEG activity in well-rested and partially sleep-deprived adolescents. Forty-seven subjects (15 – 21 years) were assigned to a well-rested (8 h sleep; 9 men, 15 women) or a sleep-deprived group (4 h sleep; 11 men, 12 women). All underwent 30 minutes of morning bright light exposure, with EEG, cognitive testing, and ratings of sleepiness and affect conducted pre- and post-intervention. Behavioral and electrophysiological changes were compared within and between groups. Associations between changes in EEG activity and behavioral outcomes were explored using correlation analyses. Bright light significantly reduced negative affect and improved Digit Span Forward task performance. No changes were observed in positive affect, subjective sleepiness, or Digit Span Backward scores. EEG analysis revealed decreased delta activity in the anterior cingulate cortex and increased beta activity in the right insula and fronto-parietal regions. Behavioral and EEG effects were similar across groups; however, only in the sleep-deprived group changes in beta activity significantly correlated with reduced negative affect. These results suggest that bright light may acutely enhance emotional state, cognitive performance, and cortical arousal in adolescents. The link between beta activity and affective improvement under sleep deprivation suggests a potential mechanism by which light supports emotional regulation.

In mammals, the suprachiasmatic nucleus (SCN) serves as the central circadian pacemaker, regulating rhythms essential for physiological processes. STAT3, a transcription factor primarily involved in immune signaling, exhibits circadian rhythmicity in SCN astrocytes. This study examined the role of STAT3 in circadian regulation across several cell types, including primary cultures of rat SCN and cortex, SCN cells and organotypic SCN slices from PER2::LUC mice, and C6 glioblastoma cells. Furthermore, the involvement of STAT3 in inflammatory responses was investigated in SCN and cortical primary cultures. STAT3 silencing enhanced Bmal1 expression across all tested cell types, disrupted Bmal1 rhythmicity in C6 cells, and reduced the amplitude of the PER2‐driven rhythm in bioluminescence in SCN primary cells and organotypic cultures. In SCN cells, STAT3 silencing also attenuated its own expression and Gfap , whereas in cortical cells, it exhibited broader effects. Under LPS stimulation, STAT3 silencing in SCN cells reduced most LPS‐induced genes, including inflammatory and oxidative stress markers, while showing variable effects in cortical cells. These findings indicate that while the role of STAT3 in the circadian clockwork appears consistent across cell types, its involvement in functional gene expression and immune responses may vary depending on the tissue and differ between SCN and cortical primary cells.

Introduction: A lack of sleep can pose a risk during military operations due to the associated decreases in physical and cognitive performance. However, fast-acting ergogenic aids, such as ammonia inhalants (AI), may temporarily mitigate those adverse effects of total sleep deprivation (TSD). Therefore, the present study aimed to investigate the acute effect of AI on cognitive and physical performance throughout 36 hours of TSD in military personnel. Methods: Eighteen male military cadets (24.1 ± 3.0 y; 79.3 ± 8.3 kg) performed 5 identical testing sessions during 36 hours of TSD (after 0 [0], 12 [–12], 24 [–24], and 36 [–36] hours of TSD), and after 8 [+8] hours of recovery sleep. During each testing session, the following assessments were conducted: Epworth sleepiness scale (ESS), simple reaction time (SRT), shooting accuracy (SA), rifle disassembling and reassembling (DAS), and countermovement jump height (JH). Heart rate (HR) was continuously monitored during the SA task, and a rating of perceived exertion (RPE) was obtained during the JH task. At each time point, tests were performed twice, either with AI or without AI as control (CON), in a counterbalanced order. Results: There was faster SRT (1.6%; p < 0.01) without increasing the number of errors, higher JH (1.5%; p < 0.01), lower RPE (9.4%; p < 0.001), and higher HR (5.0%; p < 0.001) after using AI compared to CON regardless of TSD. However, neither SA nor DAS were affected by AI or TSD (p > 0.05). Independent of AI, the SRT was slower (3.2–9.3%; p < 0.001) in the mornings (-24, +8) than in the evening (-12), JH was higher (3.0–4.7%, p < 0.001) in the evenings (-12, -36) than in the mornings (0, -24, +8), and RPE was higher (20.0–40.1%; p < 0.001) in the sleep-deprived morning (-24) than all other timepoints (0, -12, -36, +8). Furthermore, higher ESS (59.5–193.4%; p < 0.001) was reported at -24 and -36 than the rest of the time points (0, -12, and + 8). Conclusion: Although there were detrimental effects of TSD, the usage of AI did not reduce those adverse effects. However, regardless of TSD, AI did result in a short-term increase in HR, improved SRT without affecting the number of errors, and improved JH while concurrently decreasing the RPE. No changes, yet, were observed in SA and DAS. These results suggest that AI could potentially be useful in some military scenarios, regardless of sleep deprivation.

Circadian clocks regulate multiple physiological domains from molecular to behavioral levels and adjust bodily physiology to seasonal changes in day length. Circadian regulation of cellular bioenergy and immunity in the cardiovascular and muscle systems may underpin the individual diurnal differences in performance capacity during exercise. Several studies have shown diurnal differences in cardiopulmonary parameters at maximal and submaximal workloads in morning and evening circadian human phenotypes. However, the effect of seasons on these changes was not elucidated. In this study, we recruited subjects with Morningness–Eveningness Questionnaire scores corresponding to morning and evening types. Subjects underwent morning (7:00–9:00) and evening (20:00–22:00) maximal workload spiroergometry in both winter and summer seasons. We analyzed their performance time, anaerobic threshold, heart rate, and respiratory parameters. Our results suggest that evening types manifest diurnal variations in physical performance, particularly in winter. They also have slower heart rate recovery than morning types, irrespective of the time of day or season. Compared to winter, the chronotype effect on the magnitude of morning–evening differences in performance time, maximal heart rate, and anaerobic threshold onset was more significant in summer. Our data are in concordance with previous observations and confirm the difference between morning and evening types in the timing of maximum performance capacity.

All Arctic visitors have to deal with extreme conditions, including a constant high light intensity during the summer season or constant darkness during winter. The light/dark cycle serves as the most potent synchronizing signal for the biological clock, and any Arctic visitor attending those regions during winter or summer would struggle with the absence of those entraining signals. However, the inner clock can be synchronized by other zeitgebers such as physical activity, food intake, or social interactions. Here, we investigated the effect of the polar day on the circadian clock of 10 researchers attending the polar base station in the Svalbard region during the summer season. The data collected in Svalbard was compared with data obtained just before leaving for the expedition (in the Czech Republic 49.8175°N, 15.4730°E). To determine the circadian functions, we monitored activity/rest rhythm with wrist actigraphy followed by sleep diaries, melatonin rhythm in saliva, and clock gene expression (Per1, Bmal1, and Nr1D1) in buccal mucosa samples. Our data shows that the two-week stay in Svalbard delayed melatonin onset but did not affect its rhythmic secretion, and delayed the activity/rest rhythm. Furthermore, the clock gene expression displayed a higher amplitude in Svalbard compared to the amplitude detected in the Czech Republic. We hypothesize that the common daily schedule at the Svalbard expedition strengthens circadian rhythmicity even in conditions of compromised light/dark cycles. To our knowledge, this is the first study to demonstrate peripheral clock gene expression during a polar expedition.