Effects of Night Illumination on Behavior, Body Mass and Learning in Male Zebra Finches

An increase in artificial night lighting has blurred the boundaries of day and night and transformed the natural day-night environment with alteration in the temporal niche of the animals. Male zebra finches were exposed to a dim light at night (dLAN) protocol (Light: dLAN, 12L = 200 lux: 12dLAN = 5 lux) with controls on darkness at night (Light: dark, 12L = 200 lux: 12D = 0 lux) for six weeks. We assayed sleep-wake, daily behaviors, mood, and cognition, as well as changes in physiological parameters. Dim light at night increased sleep frequency, delayed sleep onset, advanced awakening latency, and caused a reduction in total sleep duration. dLAN birds did not associate (physical association) with novel object and birds spent significantly lesser time on perch with novel object as compared to LD. In colour learning task, night illuminated birds took more time to learn and made more error, compared to LD. dLAN significantly altered the 24-h daily behavioral rhythm (amplitude and acrophase) of feeding, drinking, preening, and perch-hopping behavior. In particular, birds extended their feeding hours in the nighttime under dLAN, with no difference in total food intake. Birds under dLAN increased fattening and hence significantly increased body mass. Our results show that dim light at night altered feeding rhythm, caused decrease in sleep behavior, and negatively affected learning and memory performance in male zebra finches.

CHRONO and DEC1/DEC2 compensate for lack of CRY1/CRY2 in expression of coherent circadian rhythm but not in generation of circadian oscillation in the neonatal mouse SCN

Clock genes Cry1 and Cry2, inhibitory components of core molecular feedback loop, are regarded as critical molecules for the circadian rhythm generation in mammals. A double knockout of Cry1 and Cry2 abolishes the circadian behavioral rhythm in adult mice under constant darkness. However, robust circadian rhythms in PER2::LUC expression are detected in the cultured suprachiasmatic nucleus (SCN) of Cry1/Cry2 deficient neonatal mice and restored in adult SCN by co-culture with wild-type neonatal SCN. These findings led us to postulate the compensatory molecule(s) for Cry1/Cry2 deficiency in circadian rhythm generation. We examined the roles of Chrono and Dec1/Dec2 proteins, the suppressors of Per(s) transcription similar to CRY(s). Unexpectedly, knockout of Chrono or Dec1/Dec2 in the Cry1/Cry2 deficient mice did not abolish but decoupled the coherent circadian rhythm into three different periodicities or significantly shortened the circadian period in neonatal SCN. DNA microarray analysis for the SCN of Cry1/Cry2 deficient mice revealed substantial increases in Per(s), Chrono and Dec(s) expression, indicating disinhibition of the transactivation by BMAL1/CLOCK. Here, we conclude that Chrono and Dec1/Dec2 do not compensate for absence of CRY1/CRY2 in the circadian rhythm generation but contribute to the coherent circadian rhythm expression in the neonatal mouse SCN most likely through integration of cellular circadian rhythms.

Individual differences in neural entrainment to rhythm predict spoken grammar skills in six-year-old children

Individual differences in rhythm perception skills play an important role in predicting individual differences in spoken grammar abilities, arguably because both meter and language are hierarchically-organized structures. Based on the idea that neural entrainment sustains attentional fluctuations that facilitate hierarchical processing in both domains, we hypothesized that individual differences in syntactic (grammatical) skills may be predicted by patterns of neural entrainment to musical rhythm. To test this hypothesis, we recorded neural activity using electroencephalography (EEG) while children (N = 25) listened passively to rhythmic patterns that differed in placement of the beat, using a paradigm that had previously shown to modulate beta and gamma band responses in adults. Analysis of evoked activity in these frequency bands showed that individual differences in the magnitude of neural responses to rhythm predicted variance in six-year-olds’ spoken expressive grammar abilities, over and above the contribution of their behavioral rhythm perception task performance. Variance in the EEG beta and gamma during rhythmic listening was predictive of children’s performance on items with complex structural dependencies, i.e., for which more refined grammatical abilities are required. These results reinforce the idea that mechanisms of neural entrainment to the beat may be a shared neural resource supporting hierarchical processing across music and language, and suggest a relevant brain marker of the relationship between rhythm processing and grammar abilities in elementary-school-age children, previously observed only behaviorally. These findings add to the literature on individual differences in music ability as predictors of child language and academic development.

Challenging the Integrity of Rhythmic Maternal Signals Revealed Gene-Specific Responses in the Fetal Suprachiasmatic Nuclei

During fetal stage, maternal circadian system sets the phase of the developing clock in the suprachiasmatic nuclei (SCN) via complex pathways. We addressed the issue of how impaired maternal signaling due to a disturbed environmental light/dark (LD) cycle affects the fetal SCN. We exposed pregnant Wistar rats to two different challenges – a 6-h phase shift in the LD cycle on gestational day 14, or exposure to constant light (LL) throughout pregnancy – and detected the impact on gene expression profiles in 19-day-old fetuses. The LD phase shift, which changed the maternal SCN into a transient state, caused robust downregulation of expression profiles of clock genes (Per1, Per2, and Nr1d1), clock-controlled (Dbp) genes, as well as genes involved in sensing various signals, such as c-fos and Nr3c1. Removal of the rhythmic maternal signals via exposure of pregnant rats to LL abolished the rhythms in expression of c-fos and Nr3c1 in the fetal SCN. We identified c-fos as the gene primarily responsible for sensing rhythmic maternal signals because its expression profile tracked the shifted or arrhythmic maternal SCN clock. Pathways related to the maternal rhythmic behavioral state were likely not involved in driving the c-fos expression rhythm. Instead, introduction of a behavioral rhythm to LL-exposed mothers via restricted feeding regime strengthened rhythm in Vip expression in the fetal SCN. Our results revealed for the first time that the fetal SCN is highly sensitive in a gene-specific manner to various changes in maternal signaling due to disturbances of environmental cycles related to the modern lifestyle in humans.

Using behavioral rhythms and multi-task learning to predict fine-grained symptoms of schizophrenia

Schizophrenia is a severe and complex psychiatric disorder with heterogeneous and dynamic multi-dimensional symptoms. Behavioral rhythms, such as sleep rhythm, are usually disrupted in people with schizophrenia. As such, behavioral rhythm sensing with smartphones and machine learning can help better understand and predict their symptoms. Our goal is to predict fine-grained symptom changes with interpretable models. We computed rhythm-based features from 61 participants with 6,132 days of data and used multi-task learning to predict their ecological momentary assessment scores for 10 different symptom items. By taking into account both the similarities and differences between different participants and symptoms, our multi-task learning models perform statistically significantly better than the models trained with single-task learning for predicting patients’ individual symptom trajectories, such as feeling depressed, social, and calm and hearing voices. We also found different subtypes for each of the symptoms by applying unsupervised clustering to the feature weights in the models. Taken together, compared to the features used in the previous studies, our rhythm features not only improved models’ prediction accuracy but also provided better interpretability for how patients’ behavioral rhythms and the rhythms of their environments influence their symptom conditions. This will enable both the patients and clinicians to monitor how these factors affect a patient’s condition and how to mitigate the influence of these factors. As such, we envision that our solution allows early detection and early intervention before a patient’s condition starts deteriorating without requiring extra effort from patients and clinicians.

Circadian tau differences and rhythm associations in delayed sleep–wake phase disorder and sighted non-24-hour sleep–wake rhythm disorder

Study Objectives We investigated biological and behavioral rhythm period lengths (i.e. taus) of delayed sleep–wake phase disorder (DSWPD) and non-24-hour sleep–wake rhythm disorder (N24SWD). Based on circadian phase timing (temperature and dim light melatonin onset), DSWPD participants were dichotomized into a circadian-delayed and a circadian non-delayed group to investigate etiological differences. Methods Participants with DSWPD (n = 26, 17 m, age: 21.85 ± 4.97 years), full-sighted N24SWD (n = 4, 3 m, age: 25.75 ± 4.99 years) and 18 controls (10 m, age: 23.72 ± 5.10 years) participated in an 80-h modified constant routine. An ultradian protocol of 1-h “days” in dim light, controlled conditions alternated 20-min sleep/dark periods with 40-min enforced wakefulness/light. Subjective sleepiness ratings were recorded prior to every sleep/dark opportunity and median reaction time (vigilance) was measured hourly. Obtained sleep (sleep propensity) was derived from 20-min sleep/dark opportunities to quantify hourly objective sleepiness. Hourly core body temperature was recorded, and salivary melatonin assayed to measure endogenous circadian rhythms. Rhythm data were curved using the two-component cosine model. Results Patients with DSWPD and N24SWD had significantly longer melatonin and temperature taus compared to controls. Circadian non-delayed DSWPD had normally timed temperature and melatonin rhythms but were typically sleeping at relatively late circadian phases compared to those with circadian-delayed DSWPD. Conclusions People with DSWPD and N24SWD exhibit significantly longer biological circadian rhythm period lengths compared to controls. Approximately half of those diagnosed with DSWPD do not have abnormally delayed circadian rhythm timings suggesting abnormal phase relationship between biological rhythms and behavioral sleep period or potentially conditioned sleep-onset insomnia.