Total sleep deprivation reduces top-down regulation of emotion without altering bottom-up affective processing

Sleep loss is reported to influence affective processing, causing changes in overall mood and altering emotion regulation. These aspects of affective processing are seldom investigated together, making it difficult to determine whether total sleep deprivation has a global effect on how affective stimuli and emotions are processed, or whether specific components of affective processing are affected selectively. Sixty healthy adults were recruited for an in-laboratory study and, after a monitored night of sleep and laboratory acclimation, randomly assigned to either a total sleep deprivation condition (n = 40) or a rested control condition (n = 20). Measurements of mood, vigilant attention to affective stimuli, affective working memory, affective categorization, and emotion regulation were taken for both groups. With one exception, measures of interest were administered twice: once at baseline and again 24 hours later, after the sleep deprived group had spent a night awake (working memory was assessed only after total sleep deprivation). Sleep deprived individuals experienced an overall reduction in positive affect with no significant change in negative affect. Despite the substantial decline in positive affect, there was no evidence that processing affectively valenced information was biased under total sleep deprivation. Sleep deprived subjects did not rate affective stimuli differently from rested subjects, nor did they show sleep deprivation-specific effects of affect type on vigilant attention, working memory, and categorization tasks. However, sleep deprived subjects showed less effective regulation of negative emotion. Overall, we found no evidence that total sleep deprivation biased the processing of affective stimuli in general. By contrast, total sleep deprivation appeared to reduce controlled processing required for emotion regulation.

Cardiac mitochondrial plasticity and thermal sensitivity in a fish inhabiting an artificially heated ecosystem

Some evidence suggests that cardiac mitochondrial functions might be involved in the resilience of ectotherms such as fish to environmental warming. Here, we investigated the effects of acute and chronic changes in thermal regimes on cardiac mitochondrial plasticity and thermal sensitivity in perch (Perca fluviatilis) from an artificially heated ecosystem; the “Biotest enclosure” (~25 °C), and from an adjacent area in the Baltic Sea with normal temperatures (reference, ~16 °C). We evaluated cardiac mitochondrial respiration at assay temperatures of 16 and 25 °C, as well as activities of lactate dehydrogenase (LDH) and citrate synthase (CS) in Biotest and reference perch following 8 months laboratory-acclimation to either 16 or 25 °C. While both populations exhibited higher acute mitochondrial thermal sensitivity when acclimated to their natural habitat temperatures, this sensitivity was lost when Biotest and reference fish were acclimated to 16 and 25 °C, respectively. Moreover, reference fish displayed patterns of metabolic thermal compensation when acclimated to 25 °C, whereas no changes were observed in Biotest perch acclimated to 16 °C, suggesting that cardiac mitochondrial metabolism of Biotest fish expresses local adaptation. This study highlights the adaptive responses of cardiac mitochondria to environmental warming, which can impact on fish survival and distribution in a warming climate.

Are model organisms representative for climate change research? Testing thermal tolerance in wild and laboratory zebrafish populations

Model organisms can be useful for studying climate change impacts, but it is unclear whether domestication to laboratory conditions has altered their thermal tolerance and therefore how representative of wild populations they are. Zebrafish in the wild live in fluctuating thermal environments that potentially reach harmful temperatures. In the laboratory, zebrafish have gone through four decades of domestication and adaptation to stable optimal temperatures with few thermal extremes. If maintaining thermal tolerance is costly or if genetic traits promoting laboratory fitness at optimal temperature differ from genetic traits for high thermal tolerance, the thermal tolerance of laboratory zebrafish could be hypothesized to be lower than that of wild zebrafish. Furthermore, very little is known about the thermal environment of wild zebrafish and how close to their thermal limits they live. Here, we compared the acute upper thermal tolerance (critical thermal maxima; CTmax) of wild zebrafish measured on-site in West Bengal, India, to zebrafish at three laboratory acclimation/domestication levels: wild-caught, F1 generation wild-caught and domesticated laboratory AB-WT line. We found that in the wild, CTmax increased with increasing site temperature. Yet at the warmest site, zebrafish lived very close to their thermal limit, suggesting that they may currently encounter lethal temperatures. In the laboratory, acclimation temperature appeared to have a stronger effect on CTmax than it did in the wild. The fish in the wild also had a 0.85–1.01°C lower CTmax compared to all laboratory populations. This difference between laboratory-held and wild populations shows that environmental conditions can affect zebrafish’s thermal tolerance. However, there was no difference in CTmax between the laboratory-held populations regardless of the domestication duration. This suggests that thermal tolerance is maintained during domestication and highlights that experiments using domesticated laboratory-reared model species can be appropriate for addressing certain questions on thermal tolerance and global warming impacts.

Seasonal acclimatization of brain lipidome in a eurythermal fish (Carassius carassius) is mainly determined by temperature

Crucian carp ( Carassius carassius) is an excellent vertebrate model for studies on temperature adaptation in biological excitable membranes, since the species can tolerate temperatures from 0 to +36°C. To determine how temperature affects the lipid composition of brain, the fish were acclimated for 4 wk at +30, +16, or +4°C in the laboratory, or seasonally acclimatized individuals were captured from the wild throughout the year (temperature = +1 to +23°C), and the brain glycerophospholipid and sphingolipid compositions were analyzed in detail by electrospray-ionization mass spectrometry. Numerous significant temperature-related changes were found in the molecular species composition of the membrane lipids. The most notable and novel finding was a large (∼3-fold) increase of the di-22:6n-3 phosphatidylserine and phosphatidylethanolamine species in the cold. Since the increase of 22:6n-3 in the total fatty acyl pool of the brain was small, the formation of di-22:6n-3 aminophospholipid species appears to be a specific adaptation to low temperature. Such highly unsaturated species could be needed to maintain adequate membrane fluidity in the vicinity of transporters and other integral membrane proteins. Plasmalogens increased somewhat at higher temperatures, possibly to protect membranes against oxidation. The modifications of brain lipidome during the 4-wk laboratory acclimation were, in many respects, similar to those found in the wild, which indicates that the seasonal changes observed in the wild are temperature dependent rather than induced by other environmental factors.

Critical thermal maxima of coho salmon (Oncorhynchus kisutch) fry under field and laboratory acclimation regimes

Juvenile coho salmon (Oncorhynchus kisutch) from three populations in Washington State were captured in the field and tested for critical thermal maximum (CTM). Tolerances varied among the populations (mean CTMs were 28.21, 29.13, and 29.23 °C) and exceeded published data from some laboratory tests. The population from a relatively cool stream had a lower CTM than the two populations from warmer streams. However, after the salmon had been in the laboratory for 3 months under constant, common temperature regimes, the CTMs no longer differed, indicating that the population-specific differences resulted from different acclimation regimes rather than from genetic adaptation.