Circadian rhythms and memory formation

Gerstner, Jason R.; Yin, Jingyi

doi:10.1038/nrn2881

Cited by 217 publications

(180 citation statements)

References 147 publications

(154 reference statements)

Supporting

Mentioning

174

Contrasting

Unclassified

Order By: Relevance

“…The hippocampus presumably holds a central place in cTPL behavior, perhaps not only for the storage and retrieval of time-place associated memories, but also for harboring a local timekeeping mechanism. Clock genes are expressed in all subregions of the hippocampus and thought to support temporally regulated events underlying memory processes, such as acquisition, consolidation, and retrieval (Eckel-Mahan et al 2008;Eckel-Mahan and Storm 2009;Gerstner et al 2009;Gerstner and Yin 2010;Jilg et al 2010;Kondratova et al 2010;Rawashdeh and Stehle 2010;Kondratova and Kondratov 2012). In a pilot study, we found a 26% increase in CRY2 (the protein product of the core molecular clock gene Cry2) positive cells in the hippocampal dentate gyrus of TPL-trained mice compared with homecage control mice (data not included).…”

Section: Circadian System Decline Versus Cognitive Decline With Agementioning

confidence: 95%

“…Other hallmarks are an increased fragmentation of rhythms, extended activity periods, changes in free-running period, disturbed sleep-wake rhythms, altered phase relationships, and changes in the ability to synchronize to zeitgebers (for review, see Van Someren et al 1999;Weinert 2000). Recent studies have indicated that the circadian system supports temporally regulated events underlying memory processes, such as acquisition, consolidation, and retrieval (Eckel-Mahan and Storm 2009;Gerstner et al 2009;Gerstner and Yin 2010;Jilg et al 2010;Kondratova et al 2010;Rawashdeh and Stehle 2010). It has been proposed that the aging-related flattening of circadian rhythms is causally linked to hippocampal neuropathology (Stranahan et al 2008;Kondratova and Kondratov 2012).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Time–place learning over a lifetime: absence of memory loss in trained old mice

et al. 2015

View full text Add to dashboard Cite

Time -place learning (TPL) offers the possibility to study the functional interaction between cognition and the circadian system with aging. With TPL, animals link biological significant events with the location and the time of day. This whatwhere-when type of memory provides animals with an experience-based daily schedule. Mice were tested for TPL five times throughout their lifespan and showed (re)learning from below chance level at the age of 4, 7, 12, and 18 mo. In contrast, at the age of 22 mo these mice showed preservation of TPL memory (absence of memory loss), together with deficiencies in the ability to update time-of-day information. Conversely, the majority of untrained (na€ ıve) mice at 17 mo of age were unable to acquire TPL, indicating that training had delayed TPL deficiencies in the mice trained over lifespan. Two out of seven na€ ıve mice, however, compensated for correct performance loss by adapting an alternative learning strategy that is independent of the age-deteriorating circadian system and presumably less cognitively demanding. Together, these data show the age-sensitivity of TPL, and the positive effects of repeated training over a lifetime. In addition, these data shed new light on aging-related loss of behavioral flexibility to update time-of-day information.

show abstract

Section: Circadian System Decline Versus Cognitive Decline With Agementioning

confidence: 95%

mentioning

confidence: 99%

Time–place learning over a lifetime: absence of memory loss in trained old mice

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Long-term memory consolidation such as remote fear memory formation is thought to depend on the gradual transfer of memory traces from hippocampal to cortical structures in a periodic and sleep-dependent process, which may involve the function of clock genes (40). In this study, we analyzed cognitive processing in single and double null mouse mutants of the clock modulators SHARP1 and -2.…”

Section: Discussionmentioning

confidence: 99%

Enhanced memory consolidation in mice lacking the circadian modulators Sharp1 and -2 caused by elevated Igf2 signaling in the cortex

Shahmoradi

Radyushkin

Rossner

2015

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The bHLH transcription factors SHARP1 and SHARP2 are partially redundant modulators of the circadian system. SHARP1/DEC2 has been shown to control sleep length in humans and sleep architecture is also altered in double mutant mice (S1/2 −/− ). Because of the importance of sleep for memory consolidation, we investigated the role of SHARP1 and SHARP2 in cognitive processing. S1/2 −/− mice show enhanced cortex (Cx)-dependent remote fear memory formation as well as improved reversal learning, but do not display alterations in hippocampus (Hi)-dependent recent fear memory formation. SHARP1 and SHARP2 single null mutants do not display any cognitive phenotype supporting functional redundancy of both factors. Molecular and biochemical analyses revealed elevated insulin-related growth factor 2 (IGF2) signaling and increased phosphorylation of MAPK and S6 in the Cx but not the Hi of S1/2 −/− mice. No changes were detected in single mutants. Moreover, adenoassociated virus type 2-mediated IGF2 overexpression in the anterior cingulate cortex enhanced remote fear memory formation and the analysis of forebrain-specific double null mutants of the Insulin and IGF1 receptors revealed their essential function for memory formation. Impaired fear memory formation in aged S1/2 −/− mice indicates that elevated IGF2 signaling in the long term, however, has a negative impact on cognitive processing. In summary, we conclude that the bHLH transcription factors SHARP1 and SHARP2 are involved in cognitive processing by controlling Igf2 expression and associated signaling cascades. Our analyses provide evidence that the control of sleep and memory consolidation may share common molecular mechanisms.cortex | memory consolidation | insulin-like signaling | aging | MAPK signaling T he hippocampus (Hi) and anterior cortex (ACx) have been associated with different aspects of cognitive processes controlling, for example, recent and remote long-term fear memory formation, respectively (1). Current concepts suggest that longterm fear memory consolidation involves a gradual transfer of memory traces from hippocampal networks into stable cortical modules integrated by the anterior cingulate cortex (ACC) (2). Long-term memory consolidation is considered a highly dynamic process involving different cortical areas and is thought to be shaped already during encoding, storage, but also reconsolidation processes (3, 4). The gradual transfer of memory traces from the Hi to cortical structures is thought to be dependent on different aspects of sleep (5) such as the sleep-dependent memory replay between the Hi and the cortex (6). Thus, the controls of sleep and memory consolidation appear to be interconnected processes. It is well known that many aspects of sleep-wakerelated behavior are controlled by clock genes and emerging evidence suggests an involvement of the circadian system in cognitive processes (7). Several signaling pathways have been studied in the context of hippocampal learning (8-14), among those, the circadian timing of mitogen-activated prot...

show abstract

“…Outside of the SCN there are circadian oscillators throughout the brain and periphery, and the circadian network normally functions as a complex and distributed system that imposes temporal architecture on physiology and behavior (5). There are also circadian rhythms in neurocognitive parameters (6,7) and disruption of circadian rhythms leads to cognitive impairments (8). Circadian dysfunction also impacts negatively on immune, metabolic, and cardiovascular systems (9,10).…”

mentioning

confidence: 99%

The Circadian System in Alzheimer’s Disease: Disturbances, Mechanisms, and Opportunities

Coogan

Schutová

Husung

et al. 2013

Biological Psychiatry

148

131

View full text Add to dashboard Cite

Alzheimer's disease (AD) is a devastating neurodegenerative condition associated with severe cognitive and behavioral impairments. Circadian rhythms are recurring cycles that display periods of approximately 24 hours and are driven by an endogenous circadian timekeeping system centered on the suprachiasmatic nucleus of the hypothalamus. We review the compelling evidence that circadian rhythms are significantly disturbed in AD and that such disturbance is of significant clinical importance in terms of behavioral symptoms. We also detail findings from neuropathological studies of brain areas associated with the circadian system in postmortem studies, the use of animal models of AD in the investigation of circadian processes, and the evidence that chronotherapeutic approaches aimed at bolstering weakened circadian rhythms in AD produce beneficial outcomes. We argue that further investigation in such areas is warranted and highlight areas for future research that might prove fruitful in ultimately providing new treatment options for this most serious and intractable of conditions.

show abstract

Circadian rhythms and memory formation

Cited by 217 publications

References 147 publications

Time–place learning over a lifetime: absence of memory loss in trained old mice

Time–place learning over a lifetime: absence of memory loss in trained old mice

Enhanced memory consolidation in mice lacking the circadian modulators Sharp1 and -2 caused by elevated Igf2 signaling in the cortex

The Circadian System in Alzheimer’s Disease: Disturbances, Mechanisms, and Opportunities

Contact Info

Product

Resources

About