Delayed Sleep in Winter Related to Natural Daylight Exposure among Arctic Day Workers.

Natural daylight exposures in arctic regions vary substantially across seasons. Negative consequences have been observed in self-reports of sleep and daytime functions during the winter but have rarely been studied in detail. The focus of the present study set out to investigate sleep seasonality among indoor workers using objective and subjective measures. Sleep seasonality among daytime office workers (n = 32) in Kiruna (Sweden, 67.86° N, 20.23° E) was studied by comparing the same group of workers in a winter and summer week, including work and days off at the weekend, using actigraphs (motion loggers) and subjective ratings of alertness and mood. Actigraph analyses showed delayed sleep onset of 39 min in winter compared to the corresponding summer week (p < 0.0001) and shorter weekly sleep duration by 12 min (p = 0.0154). A delay of mid-sleep was present in winter at workdays (25 min, p < 0.0001) and more strongly delayed during days off (46 min, p < 0.0001). Sleepiness levels were higher in winter compared to summer (p < 0.05). Increased morning light exposure was associated with earlier mid-sleep (p < 0.001), while increased evening light exposure was associated with delay (p < 0.01). This study confirms earlier work that suggests that lack of natural daylight delays the sleep/wake cycle in a group of indoor workers, despite having access to electric lighting. Photic stimuli resulted in a general advanced sleep/wake rhythm during summer and increased alertness levels.

Comprehensive analysis of tissue preservation and recording quality from chronic multielectrode implants.

Multielectrodes have been used with great success to simultaneously record the activity of neuronal populations in awake, behaving animals. In particular, there is great promise in the use of this technique to allow the control of neuroprosthetic devices by human patients. However, it is crucial to fully characterize the tissue response to the chronic implants in animal models ahead of the initiation of human clinical trials. Here we evaluated the effects of unilateral multielectrode implants on the motor cortex of rats weekly recorded for 1-6 months using several histological methods to assess metabolic markers, inflammatory response, immediate-early gene (IEG) expression, cytoskeletal integrity and apoptotic profiles. We also investigated the correlations between each of these features and firing rates, to estimate the impact of post-implant time on neuronal recordings. Overall, limited neuronal loss and glial activation were observed on the implanted sites. Reactivity to enzymatic metabolic markers and IEG expression were not significantly different between implanted and non-implanted hemispheres. Multielectrode recordings remained viable for up to 6 months after implantation, and firing rates correlated well to the histochemical and immunohistochemical markers. Altogether, our results indicate that chronic tungsten multielectrode implants do not substantially alter the histological and functional integrity of target sites in the cerebral cortex.

Neuronal activity in the primary somatosensory thalamocortical loop is modulated by reward contingency during tactile discrimination.

Delayed-response sensory discrimination is believed to require primary sensory thalamus and cortex for early stimulus identification and higher-order forebrain regions for the late association of stimuli with rewarded motor responses. Here we investigate neuronal responses in the rat primary somatosensory cortex (S1) and ventral posterior medial nucleus of the thalamus (VPM) during a tactile discrimination task that requires animals to associate two different tactile stimuli with two corresponding choices of spatial trajectory to be rewarded. To manipulate reward expectation, neuronal activity observed under regular reward contingency (CR) was compared with neuronal activity recorded during freely rewarded (FR) trials, in which animals obtained reward regardless of their choice of spatial trajectory. Across-trial firing rates of S1 and VPM neurons varied according to the reward contingency of the task. Analysis of neuronal ensemble activity by an artificial neural network showed that stimulus-related information in S1 and VPM increased from stimulus sampling to reward delivery in CR trials but decreased to chance levels when animals performed FR trials, when stimulus discrimination was irrelevant for task execution. Neuronal ensemble activity in VPM was only correlated with task performance during stimulus presentation. In contrast, S1 neuronal activity was highly correlated with task performance long after stimulus removal, a relationship that peaked during the 300 ms that preceded reward delivery. Together, our results indicate that neuronal activity in the primary somatosensory thalamocortical loop is strongly modulated by reward contingency.

Novel experience induces persistent sleep-dependent plasticity in the cortex but not in the hippocampus.

Episodic and spatial memories engage the hippocampus during acquisition but migrate to the cerebral cortex over time. We have recently proposed that the interplay between slow-wave (SWS) and rapid eye movement (REM) sleep propagates recent synaptic changes from the hippocampus to the cortex. To test this theory, we jointly assessed extracellular neuronal activity, local field potentials (LFP), and expression levels of plasticity-related immediate-early genes (IEG) arc and zif-268 in rats exposed to novel spatio-tactile experience. Post-experience firing rate increases were strongest in SWS and lasted much longer in the cortex (hours) than in the hippocampus (minutes). During REM sleep, firing rates showed strong temporal dependence across brain areas: cortical activation during experience predicted hippocampal activity in the first post-experience hour, while hippocampal activation during experience predicted cortical activity in the third post-experience hour. Four hours after experience, IEG expression was specifically upregulated during REM sleep in the cortex, but not in the hippocampus. Arc gene expression in the cortex was proportional to LFP amplitude in the spindle-range (10-14 Hz) but not to firing rates, as expected from signals more related to dendritic input than to somatic output. The results indicate that hippocampo-cortical activation during waking is followed by multiple waves of cortical plasticity as full sleep cycles recur. The absence of equivalent changes in the hippocampus may explain its mnemonic disengagement over time.