Pub Date : 2025-05-01Epub Date: 2025-05-16DOI: 10.1016/j.nbscr.2025.100128
Mark R. Opp , Rachel K. Rowe , Hans P.A. Van Dongen
{"title":"Foreword: Festschrift in honor of JM Krueger's research","authors":"Mark R. Opp , Rachel K. Rowe , Hans P.A. Van Dongen","doi":"10.1016/j.nbscr.2025.100128","DOIUrl":"10.1016/j.nbscr.2025.100128","url":null,"abstract":"","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100128"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01Epub Date: 2025-04-25DOI: 10.1016/j.nbscr.2025.100123
Maria I. Smirnova , Ning Quan
Adult hippocampal neurogenesis (AHN) plays a critical role in cognition and emotional regulation. Recent studies have linked compromised AHN to numerous neurological and psychological disorders. The actions of the inflammatory cytokine interleukin-1 (IL-1) have been found to suppress AHN and antagonism of IL-1 signaling has been advocated as a therapeutic strategy for the treatment of neurodegenerative diseases and affective disorders. On the other hand, work from Jim Krueger's group revealed the physiological function of IL-1 in brain homeostasis, indicating the potential downside of IL-1 blockade. Current literature also shows AHN participates in normal functions of the brain in parallel to IL-1. This mini-review analyzes how IL-1 might positively or negatively modulate AHN and the implications of the relationship between IL-1 and AHN on health and disease. Specifically, we will highlight the parallels between IL-1 signaling and AHN in physiological and disease states. We propose that IL-1 signaling modulates AHN in a context-dependent manner; whereas its elevated signaling impairs neurogenesis and contributes to neurological and psychiatric disorders, its physiological role suggests potential therapeutic benefits of IL-1 antagonism must consider the preservation of the beneficial actions of IL-1.
{"title":"Modulation of adult hippocampal neurogenesis by interleukin 1 signaling","authors":"Maria I. Smirnova , Ning Quan","doi":"10.1016/j.nbscr.2025.100123","DOIUrl":"10.1016/j.nbscr.2025.100123","url":null,"abstract":"<div><div>Adult hippocampal neurogenesis (AHN) plays a critical role in cognition and emotional regulation. Recent studies have linked compromised AHN to numerous neurological and psychological disorders. The actions of the inflammatory cytokine interleukin-1 (IL-1) have been found to suppress AHN and antagonism of IL-1 signaling has been advocated as a therapeutic strategy for the treatment of neurodegenerative diseases and affective disorders. On the other hand, work from Jim Krueger's group revealed the physiological function of IL-1 in brain homeostasis, indicating the potential downside of IL-1 blockade. Current literature also shows AHN participates in normal functions of the brain in parallel to IL-1. This mini-review analyzes how IL-1 might positively or negatively modulate AHN and the implications of the relationship between IL-1 and AHN on health and disease. Specifically, we will highlight the parallels between IL-1 signaling and AHN in physiological and disease states. We propose that IL-1 signaling modulates AHN in a context-dependent manner; whereas its elevated signaling impairs neurogenesis and contributes to neurological and psychiatric disorders, its physiological role suggests potential therapeutic benefits of IL-1 antagonism must consider the preservation of the beneficial actions of IL-1.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100123"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01Epub Date: 2025-04-02DOI: 10.1016/j.nbscr.2025.100117
Hans P.A. Van Dongen
The research of JM Krueger and colleagues, focusing on sleep organization as a means to elucidate sleep function, led to critical insights as to why we sleep. Krueger posited that, fundamentally, sleep occurs locally at the level of neuronal/glial assemblies (small networks of neurons and glia) and that the expression of sleep in these assemblies is dependent on their prior use. Neuronal/glial assemblies serve as units of information processing, which consumes energy and increases entropy so that the energy available for further information processing is use-dependently depleted. According to the laws of physics, when energy drops to a lower bound relative to entropy, information processing ceases – which results in local quiescence and locally reduced consciousness and manifests as use-dependent local sleep. The physics-based nature of local sleep implies that it is inevitable, has neither function nor purpose, and is by itself not subject to biology-based evolutionary shaping. But uncontrolled local sleep compromises vigilance and is a threat to safety, which needs to be addressed to ensure survival. This can be accomplished by preemptively regulating sleep at a more global level and in a way that is adapted to the organism's temporal, environmental and ecological niche. Such global sleep allows for energy resupply (through biological processes not unique to sleep) across many neuronal/glial assemblies simultaneously while the organism is relatively safe. Thus, global sleep regulation could be the biology-based adaptation to the physics-based problem of use-dependent local sleep intrusions into wakefulness. Global sleep precludes niche exploitation and thus comes at an opportunity cost – but, unlike local sleep, the regulation of global sleep is subject to evolutionary shaping and amenable to species-specific optimization. Furthermore, a variety of ancillary functions may be served during global sleep to retroactively address biological needs that arose from prior wakefulness. However, serving these functions may be merely opportunistic, as the temporal dynamics of global sleep regulation appear to be proactive rather than retroactive, prioritizing alignment of global sleep and wake timing with the organism's ecological niche. Regardless, the costs of use-dependent local sleep and the management thereof through global sleep regulation are likely to be outweighed by the evolutionary benefit of the presumed source of the local sleep problem – that is, information processing capability, or cognition. In essence, therefore, sleep may just be the unavoidable, but worthwhile, price we pay for cognition.
{"title":"Local versus global sleep organization and the quest to determine sleep function","authors":"Hans P.A. Van Dongen","doi":"10.1016/j.nbscr.2025.100117","DOIUrl":"10.1016/j.nbscr.2025.100117","url":null,"abstract":"<div><div>The research of JM Krueger and colleagues, focusing on sleep organization as a means to elucidate sleep function, led to critical insights as to why we sleep. Krueger posited that, fundamentally, sleep occurs locally at the level of neuronal/glial assemblies (small networks of neurons and glia) and that the expression of sleep in these assemblies is dependent on their prior use. Neuronal/glial assemblies serve as units of information processing, which consumes energy and increases entropy so that the energy available for further information processing is use-dependently depleted. According to the laws of physics, when energy drops to a lower bound relative to entropy, information processing ceases – which results in local quiescence and locally reduced consciousness and manifests as <em>use-dependent local sleep</em>. The physics-based nature of local sleep implies that it is inevitable, has neither function nor purpose, and is by itself not subject to biology-based evolutionary shaping. But uncontrolled local sleep compromises vigilance and is a threat to safety, which needs to be addressed to ensure survival. This can be accomplished by preemptively regulating sleep at a more global level and in a way that is adapted to the organism's temporal, environmental and ecological niche. Such global sleep allows for energy resupply (through biological processes not unique to sleep) across many neuronal/glial assemblies simultaneously while the organism is relatively safe. Thus, <em>global sleep regulation</em> could be the biology-based adaptation to the physics-based problem of use-dependent local sleep intrusions into wakefulness. Global sleep precludes niche exploitation and thus comes at an opportunity cost – but, unlike local sleep, the regulation of global sleep is subject to evolutionary shaping and amenable to species-specific optimization. Furthermore, a variety of ancillary functions may be served during global sleep to retroactively address biological needs that arose from prior wakefulness. However, serving these functions may be merely opportunistic, as the temporal dynamics of global sleep regulation appear to be proactive rather than retroactive, prioritizing alignment of global sleep and wake timing with the organism's ecological niche. Regardless, the costs of use-dependent local sleep and the management thereof through global sleep regulation are likely to be outweighed by the evolutionary benefit of the presumed source of the local sleep problem – that is, information processing capability, or cognition. In essence, therefore, sleep may just be the unavoidable, but worthwhile, price we pay for cognition.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100117"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01Epub Date: 2025-02-27DOI: 10.1016/j.nbscr.2025.100116
David E. Ehichioya , Ishrat Masud , S.K. Tahajjul Taufique , Melody Shen , Sofia Farah , Shin Yamazaki
Circadian pacemakers orchestrate behavioral and physiological rhythms, enabling organisms to anticipate daily reoccurring environmental events such as light and dark, temperature changes, and food availability. When nocturnal rodents are subjected to time-restricted feeding during the day, they typically display food anticipatory activity several hours before mealtime. Upon releasing mice to ad libitum feeding, this anticipatory activity is abolished immediately but, following food deprivation, reappears at approximately the same time. However, the mechanism by which rodents retain this time memory of food availability during ad libitum feeding has remained elusive. We utilized the open-source Feeding Experimentation Device 3 (FED3) to measure food-seeking nose-poking behavior. We programmed the FED3 to dispense a pellet by a single left nose-poke, but not by right poke. During daytime restricted feeding, mice exhibited strong anticipatory nose-poking a few hours prior to the daytime meal in both rewarded left and unrewarded right pokes. In addition, mice also exhibited elevation of both rewarded and unrewarded pokes at night, coinciding with mice's previous habitual feeding time. Following ad libitum feeding, rewarded daytime nose-poking gradually moved back to habitual nighttime. However, following food deprivation, anticipatory poking immediately reappeared during the day and night, coinciding with the times of previous daytime restricted feeding and nighttime habitual feeding. Under ad libitum feeding, db/db mice didn't exhibit a clear daily rhythm in food intake. However, these mice exhibited robust food anticipation in both nose-pokes and activity during daytime restricted feeding. Following release back to ad libitum feeding, db/db mice poked sporadically during the day and night, and following food deprivation, anticipation promptly reappeared. These data suggest that there are at least two oscillators underlying food anticipation: one oscillator with a phase that changes according to food availability, and another oscillator with a phase unaffected by feeding conditions. In db/db mice, the first oscillator is likely impaired, and the second oscillator is unaffected.
{"title":"Multiple oscillators underlie circadian food anticipation in mice","authors":"David E. Ehichioya , Ishrat Masud , S.K. Tahajjul Taufique , Melody Shen , Sofia Farah , Shin Yamazaki","doi":"10.1016/j.nbscr.2025.100116","DOIUrl":"10.1016/j.nbscr.2025.100116","url":null,"abstract":"<div><div>Circadian pacemakers orchestrate behavioral and physiological rhythms, enabling organisms to anticipate daily reoccurring environmental events such as light and dark, temperature changes, and food availability. When nocturnal rodents are subjected to time-restricted feeding during the day, they typically display food anticipatory activity several hours before mealtime. Upon releasing mice to ad libitum feeding, this anticipatory activity is abolished immediately but, following food deprivation, reappears at approximately the same time. However, the mechanism by which rodents retain this time memory of food availability during ad libitum feeding has remained elusive. We utilized the open-source Feeding Experimentation Device 3 (FED3) to measure food-seeking nose-poking behavior. We programmed the FED3 to dispense a pellet by a single left nose-poke, but not by right poke. During daytime restricted feeding, mice exhibited strong anticipatory nose-poking a few hours prior to the daytime meal in both rewarded left and unrewarded right pokes. In addition, mice also exhibited elevation of both rewarded and unrewarded pokes at night, coinciding with mice's previous habitual feeding time. Following ad libitum feeding, rewarded daytime nose-poking gradually moved back to habitual nighttime. However, following food deprivation, anticipatory poking immediately reappeared during the day and night, coinciding with the times of previous daytime restricted feeding and nighttime habitual feeding. Under ad libitum feeding, db/db mice didn't exhibit a clear daily rhythm in food intake. However, these mice exhibited robust food anticipation in both nose-pokes and activity during daytime restricted feeding. Following release back to ad libitum feeding, db/db mice poked sporadically during the day and night, and following food deprivation, anticipation promptly reappeared. These data suggest that there are at least two oscillators underlying food anticipation: one oscillator with a phase that changes according to food availability, and another oscillator with a phase unaffected by feeding conditions. In db/db mice, the first oscillator is likely impaired, and the second oscillator is unaffected.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100116"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143550080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01Epub Date: 2024-11-28DOI: 10.1016/j.nbscr.2024.100108
Gisele A. Oda
Chronobiology experiments often reveal intriguing non-linear phenomena, which require mathematical models and computer simulations for their interpretation. One example is shown here, where the two circadian oscillators located in the eyes of the mollusk Bulla gouldiana were isolated and measured in vitro. By maintaining one eye under control conditions and manipulating the period of the second eye, Page and Nalovic (1992) obtained a diversity of results, including synchronized and desynchronized eyes, associated to weak coupling and period differences. A subset of eye pairs, however, showed increasing phase angle followed by phase jumps. These occur and have been satisfactorily modeled in more complex systems where two zeitgebers play clear entraining roles. However, simulations of a simple model of free-running, two mutually coupled limit-cycle oscillators with unilateral change in oscillator period failed completely to reproduce these phase jumps. Here we explain how phase jumps arise in two-zeitgeber systems and then show the closest but unsatisfying, intermediate model that was fit to the Bulla system.
{"title":"One interesting and elusive two-coupled oscillator problem","authors":"Gisele A. Oda","doi":"10.1016/j.nbscr.2024.100108","DOIUrl":"10.1016/j.nbscr.2024.100108","url":null,"abstract":"<div><div>Chronobiology experiments often reveal intriguing non-linear phenomena, which require mathematical models and computer simulations for their interpretation. One example is shown here, where the two circadian oscillators located in the eyes of the mollusk <em>Bulla gouldiana</em> were isolated and measured <em>in vitro</em>. By maintaining one eye under control conditions and manipulating the period of the second eye, Page and Nalovic (1992) obtained a diversity of results, including synchronized and desynchronized eyes, associated to weak coupling and period differences. A subset of eye pairs, however, showed increasing phase angle followed by phase jumps. These occur and have been satisfactorily modeled in more complex systems where two zeitgebers play clear entraining roles. However, simulations of a simple model of free-running, two mutually coupled limit-cycle oscillators with unilateral change in oscillator period failed completely to reproduce these phase jumps. Here we explain how phase jumps arise in two-zeitgeber systems and then show the closest but unsatisfying, intermediate model that was fit to the <em>Bulla</em> system.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100108"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11665366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01Epub Date: 2025-05-14DOI: 10.1016/j.nbscr.2025.100126
Fernando Bravo-González , Mario Eduardo Acosta-Hernández , Hiram Tendilla-Beltrán , Gonzalo Flores , Fabio García-García
Sleep loss is associated with a potential risk of using drugs such as cocaine, methamphetamines, and alcohol. Recently, our group showed that chronic sleep restriction (CSR) for 7 days/4 h induces a significant increase in ethanol intake and delta FosB immunoreactivity in the rat's prefrontal cortex. However, whether CSR promotes changes in structural plasticity that explain ethanol consumption is unknown. Therefore, the present study aimed to determine if CSR induces changes in the dendritic length, branching of the dendritic tree, and spine morphology of the pyramidal neurons from the prelimbic cortex and whether these structural changes are associated with ethanol consumption. For this purpose, adult male Wistar rats were divided into four experimental groups: control, CSR for 7 days/4 h daily, CSR + ethanol exposure, and ethanol exposure. The two-bottle free-choice paradigm was used to measure ethanol intake, and the gentle handling method was used for CSR. At the end of the experiment, the rats were euthanized, and their brains were dissected and processed by Golgi-Cox staining. Sholl analysis was used to characterize structural plasticity. Results show that CSR induced an increase in the ethanol index preference. In addition, ethanol intake and ethanol + CSR increased the total dendritic length, dendritic tree branching, and mushroom spines in prelimbic cortex neurons. In conclusion, changes in structural plasticity associated with CSR and continuous access to ethanol may translate into neuroadaptive changes that favor drug preference and subsequently reinforce addictive behavior.
{"title":"Effect of chronic sleep restriction on ethanol preference and cortical structural plasticity","authors":"Fernando Bravo-González , Mario Eduardo Acosta-Hernández , Hiram Tendilla-Beltrán , Gonzalo Flores , Fabio García-García","doi":"10.1016/j.nbscr.2025.100126","DOIUrl":"10.1016/j.nbscr.2025.100126","url":null,"abstract":"<div><div>Sleep loss is associated with a potential risk of using drugs such as cocaine, methamphetamines, and alcohol. Recently, our group showed that chronic sleep restriction (CSR) for 7 days/4 h induces a significant increase in ethanol intake and delta FosB immunoreactivity in the rat's prefrontal cortex. However, whether CSR promotes changes in structural plasticity that explain ethanol consumption is unknown. Therefore, the present study aimed to determine if CSR induces changes in the dendritic length, branching of the dendritic tree, and spine morphology of the pyramidal neurons from the prelimbic cortex and whether these structural changes are associated with ethanol consumption. For this purpose, adult male Wistar rats were divided into four experimental groups: control, CSR for 7 days/4 h daily, CSR + ethanol exposure, and ethanol exposure. The two-bottle free-choice paradigm was used to measure ethanol intake, and the gentle handling method was used for CSR. At the end of the experiment, the rats were euthanized, and their brains were dissected and processed by Golgi-Cox staining. Sholl analysis was used to characterize structural plasticity. Results show that CSR induced an increase in the ethanol index preference. In addition, ethanol intake and ethanol + CSR increased the total dendritic length, dendritic tree branching, and mushroom spines in prelimbic cortex neurons. In conclusion, changes in structural plasticity associated with CSR and continuous access to ethanol may translate into neuroadaptive changes that favor drug preference and subsequently reinforce addictive behavior.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"18 ","pages":"Article 100126"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-09-19DOI: 10.1016/j.nbscr.2024.100106
Ayano Shiba , Paul de Goede , Roberta Tandari , Ewout Foppen , Nikita L. Korpel , Tom V. Coopmans , Tom P. Hellings , Merel W. Jansen , Annelou Ruitenberg , Wayne I.G.R. Ritsema , Chun-Xia Yi , Joram D. Mul , Dirk Jan Stenvers , Andries Kalsbeek
Circadian disruption is an important factor driving the current-day high prevalence of obesity and type-2 diabetes. While the impact of incorrect timing of caloric intake on circadian disruption is widely acknowlegded, the contribution of incorrect timing of physical activity remains relatively understudied. Here, we modeled the incorrect timing of physical activity in nightshift workers in male Wistar rats, by restricting running wheel access to the innate inactive (light) phase (LR). Controls included no wheel access (NR); access only during the innate active (dark) period (DR); or unrestricted (ad libitum) access (ALR). LR did not shift the phase of the muscle or liver clock, but dampened the muscle clock amplitude. As our previous study demonstrated that light-phase restricted feeding did shift the liver clock, but made the muscle clock arrhythmic, we next combined the time restriction of wheel and food access to either the light phase (LRLF) or dark phase (DRDF). LRLF produced a ∼12 h shift in the majority of clock gene rhythms in both skeletal muscle and liver. On the other hand, DRDF was most effective in reducing body weight and the accumulation of fat mass. Therefore, in order to shift the muscle clock in male Wistar rats, synergy between the timing of feeding and physical activity is necessary. These findings may contribute to further improve the design of lifestyle strategies that try to limit metabolic misalignment caused by circadian disruption.
{"title":"Synergy between time-restricted feeding and time-restricted running is necessary to shift the muscle clock in male wistar rats","authors":"Ayano Shiba , Paul de Goede , Roberta Tandari , Ewout Foppen , Nikita L. Korpel , Tom V. Coopmans , Tom P. Hellings , Merel W. Jansen , Annelou Ruitenberg , Wayne I.G.R. Ritsema , Chun-Xia Yi , Joram D. Mul , Dirk Jan Stenvers , Andries Kalsbeek","doi":"10.1016/j.nbscr.2024.100106","DOIUrl":"10.1016/j.nbscr.2024.100106","url":null,"abstract":"<div><div>Circadian disruption is an important factor driving the current-day high prevalence of obesity and type-2 diabetes. While the impact of incorrect timing of caloric intake on circadian disruption is widely acknowlegded, the contribution of incorrect timing of physical activity remains relatively understudied. Here, we modeled the incorrect timing of physical activity in nightshift workers in male Wistar rats, by restricting running wheel access to the innate inactive (light) phase (LR). Controls included no wheel access (NR); access only during the innate active (dark) period (DR); or unrestricted (<em>ad libitum</em>) access (ALR). LR did not shift the phase of the muscle or liver clock, but dampened the muscle clock amplitude. As our previous study demonstrated that light-phase restricted feeding did shift the liver clock, but made the muscle clock arrhythmic, we next combined the time restriction of wheel and food access to either the light phase (LRLF) or dark phase (DRDF). LRLF produced a ∼12 h shift in the majority of clock gene rhythms in both skeletal muscle and liver. On the other hand, DRDF was most effective in reducing body weight and the accumulation of fat mass. Therefore, in order to shift the muscle clock in male Wistar rats, synergy between the timing of feeding and physical activity is necessary. These findings may contribute to further improve the design of lifestyle strategies that try to limit metabolic misalignment caused by circadian disruption.</div></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"17 ","pages":"Article 100106"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S245199442400004X/pdfft?md5=55f77d77b927aa3fd8aec6e4581f4bd4&pid=1-s2.0-S245199442400004X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142314481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-07-14DOI: 10.1016/j.nbscr.2024.100105
Miranda M. Lim, Lucia Peixoto, Matthew S. Kayser, Christopher S. Colwell
{"title":"Development of sleep and circadian rhythms: Function and dysfunction","authors":"Miranda M. Lim, Lucia Peixoto, Matthew S. Kayser, Christopher S. Colwell","doi":"10.1016/j.nbscr.2024.100105","DOIUrl":"10.1016/j.nbscr.2024.100105","url":null,"abstract":"","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"17 ","pages":"Article 100105"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141694909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-01Epub Date: 2024-03-26DOI: 10.1016/j.nbscr.2024.100103
Alexis N. Jameson , Justin K. Siemann , Carrie A. Grueter , BradA. Grueter , Douglas G. McMahon
Day length, or photoperiod, is a reliable environmental cue encoded by the brain's circadian clock that indicates changing seasons and induces seasonal biological processes. In humans, photoperiod, age, and sex have been linked to seasonality in neuropsychiatric disorders, as seen in Seasonal Affective Disorder, Major Depressive Disorder, and Bipolar Disorder. The nucleus accumbens is a key locus for the regulation of motivated behaviors and neuropsychiatric disorders. Using periadolescent and young adult male and female mice, here we assessed photoperiod's effect on serotonin and dopamine tissue content in the nucleus accumbens core, as well as on accumbal synaptic dopamine release and uptake. We found greater serotonin and dopamine tissue content in the nucleus accumbens from young adult mice raised in a Short winter-like photoperiod. In addition, dopamine release and clearance were greater in the nucleus accumbens from young adult mice raised in a Long summer-like photoperiod. Importantly, we found that photoperiod's effects on accumbal dopamine tissue content and release were sex-specific to young adult females. These findings support that in mice there are interactions across age, sex, and photoperiod that impact critical monoamine neuromodulators in the nucleus accumbens which may provide mechanistic insight into the age and sex dependencies in seasonality of neuropsychiatric disorders in humans.
{"title":"Effects of age and sex on photoperiod modulation of nucleus accumbens monoamine content and release in adolescence and adulthood","authors":"Alexis N. Jameson , Justin K. Siemann , Carrie A. Grueter , BradA. Grueter , Douglas G. McMahon","doi":"10.1016/j.nbscr.2024.100103","DOIUrl":"https://doi.org/10.1016/j.nbscr.2024.100103","url":null,"abstract":"<div><p>Day length, or photoperiod, is a reliable environmental cue encoded by the brain's circadian clock that indicates changing seasons and induces seasonal biological processes. In humans, photoperiod, age, and sex have been linked to seasonality in neuropsychiatric disorders, as seen in Seasonal Affective Disorder, Major Depressive Disorder, and Bipolar Disorder. The nucleus accumbens is a key locus for the regulation of motivated behaviors and neuropsychiatric disorders. Using periadolescent and young adult male and female mice, here we assessed photoperiod's effect on serotonin and dopamine tissue content in the nucleus accumbens core, as well as on accumbal synaptic dopamine release and uptake. We found greater serotonin and dopamine tissue content in the nucleus accumbens from young adult mice raised in a Short winter-like photoperiod. In addition, dopamine release and clearance were greater in the nucleus accumbens from young adult mice raised in a Long summer-like photoperiod. Importantly, we found that photoperiod's effects on accumbal dopamine tissue content and release were sex-specific to young adult females. These findings support that in mice there are interactions across age, sex, and photoperiod that impact critical monoamine neuromodulators in the nucleus accumbens which may provide mechanistic insight into the age and sex dependencies in seasonality of neuropsychiatric disorders in humans.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"16 ","pages":"Article 100103"},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2451994424000014/pdfft?md5=7e9b52ffbf8421282f84bc3195a513c5&pid=1-s2.0-S2451994424000014-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140309605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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