Time-of-day affects expression of hippocampal markers for ischemic damage induced by global ischemia

Tischkau, Shelley A.; Cohen, Jared; Stark, Jamie T.; Gross, David R.; Bottum, Kathleen M.

doi:10.1016/j.expneurol.2007.09.003

Cited by 49 publications

(33 citation statements)

References 52 publications

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“…Interestingly, a time-of-day dependence in learning and memory and in its cellular correlate, long term potentiation (LTP) of synaptic transmission, has been observed in several species (Chaudhury and Colwell, 2002;Sakai et al, 2004;Valentinuzzi et al, 2004;Chaudhury et al, 2005;Lyons et al, 2005Lyons et al, , 2006. Although disintegration of the mammalian circadian system affects learning (Ruby et al, 2008), information on the molecular signatures and dynamics, in this context is sparse at present (Tischkau et al, 2007;Eckel-Mahan et al, 2008;Feillet et al, 2008).…”

Section: Introductionmentioning

confidence: 98%

Temporal dynamics of mouse hippocampal clock gene expression support memory processing

et al. 2009

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Hippocampal plasticity and mnemonic processing exhibit a striking time-of-day dependence and likely implicate a temporally structured replay of memory traces. Molecular mechanisms fulfilling the requirements of sensing time and capturing time-related information are coded in dynamics of so-called clock genes and their protein products, first discovered and described in the hypothalamic suprachiasmatic nucleus. Using real-time PCR and immunohistochemical analyses, we show that in wildtype mice core clock components (mPer1/PER1, mPer2/PER2, mCry1/CRY1, mCry2/CRY2, mClock/CLOCK, mBmal1/BMAL1) are expressed in neurons of all subregions of the hippocampus in a time-locked fashion over a 24-h (diurnal) day/night cycle. Temporal profiling of these transcriptional regulators reveals distinct and parallel peaks, at times when memory traces are usually formed and/or consolidated. The coordinated rhythmic expression of hippocampal clock gene expression is greatly disordered in mice deficient for the clock gene mPer1, a key player implicated in both, maintenance and adaptative plasticity of circadian clocks. Moreover, Per1-knockout animals are severely handicapped in a hippocampus-dependent long-term spatial learning paradigm. We propose that the dynamics of hippocampal clock gene expression imprint a temporal structure on memory processing and shape at the same time the efficacy of behavioral learning.

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Section: Introductionmentioning

confidence: 98%

Temporal dynamics of mouse hippocampal clock gene expression support memory processing

et al. 2009

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“…Bmal1 KO mice do not exhibit circadian rhythms, 9 and exhibit a number of sleep phenotypes including hypersomnia and an impaired ability to recover from sleep loss (> 2h additional spontaneous sleep/day vs. wild-type C57 mice). 10 The Bmal1 KO allowed us to examine if the neuroprotective effect of remote preconditioning, pii: sp-00070- 16 http://dx.doi.org/10.5665/sleep.6238…”

Section: Introductionmentioning

confidence: 99%

Sleep Is Critical for Remote Preconditioning-Induced Neuroprotection

Brager

Yang

Ehlen

et al. 2016

Sleep

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Study Objectives: Episodes of brief limb ischemia (remote preconditioning) in mice induce tolerance to modeled ischemic stroke (focal brain ischemia). Since stroke outcomes are in part dependent on sleep-wake history, we sought to determine if sleep is critical for the neuroprotective effect of limb ischemia. Methods: EEG/EMG recording electrodes were implanted in mice. After a 24 h baseline recording, limb ischemia was induced by tightening an elastic band around the left quadriceps for 10 minutes followed by 10 minutes of release for two cycles. Two days following remote preconditioning, a second 24 h EEG/EMG recording was completed and was immediately followed by a 60-minute suture occlusion of the middle cerebral artery (modeled ischemic stroke). This experiment was then repeated in a model of circadian and sleep abnormalities (Bmal1 knockout [KO] mice sleep 2 h more than wild-type littermates). Brain infarction was determined by vital dye staining, and sleep was assessed by trained identification of EEG/EMG recordings. Results: Two days after limb ischemia, wild-type mice slept an additional 2.4 h. This additional sleep was primarily comprised of non-rapid eye movement (NREM) sleep during the middle of the light-phase (i.e., naps). Repeating the experiment but preventing increases in sleep after limb ischemia abolished tolerance to ischemic stroke. In Bmal1 knockout mice, remote preconditioning did not increase daily sleep nor provide tolerance to subsequent focal ischemia. Conclusions: These results suggest that sleep induced by remote preconditioning is both sufficient and necessary for its neuroprotective effects on stroke outcome.

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“…The expression of Bmal1 and Cry1 is deregulated in mice with trauma c brain injury [257]. Stroke pa ents o en exhibit disorders of the sleep-wake cycle a er the incident [258,259]. Neuronal suscep bility to ischaemia was found to be regulated by mechanisms directly dependent on the circadian clock [254].…”

Section: Genotype-phenotype Correlations For Mutations and Polymorphimentioning

confidence: 99%

“…Per1-deficient mouse models with cerebral ischaemia exhibited higher rates of neuronal injury than similarly injured wild type controls [260]. Cerebral ischemia induced at different mes in the 24-h cycle resulted in differen al levels of expression of ini ator caspase-8 and -9 and executor caspase-3 [258]. Ischemic injury is associated with genera on of very high levels of oxida ve damage in DNA at the site of the lesion.…”

Section: Genotype-phenotype Correlations For Mutations and Polymorphimentioning

confidence: 99%

DNA damage and the circadian clock

Chakarov¹,

Petkova²,

Russev³

et al. 2014

Biodiscovery

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The role of the circadian clock has already been demonstrated for virtually all physiological processes, but it was only recently shown that cells were more sensi ve to DNA damage at specific mes of the day; that the peak of synthesis of mRNA and proteins of genes coding for products involved directly or indirectly in DNA repair was differen ally med in different ssues; and that the growth of some types of cancer followed a circadian pa ern. The paper reviews the specifici es of the clockwork mechanism in living cells associated with repair of DNA damage with regards to its role in ageing and carcinogenesis. The role of heritable polymorhisms and soma c muta ons in the risk for development of common diseases (cancer, but also other types of diseases and condi ons, such as obesity and metabolic syndrome), their course and the possible outcomes is reviewed in animal models and in man. The circadian oscilla ons in the levels of major proteins of DNA-damage related signalling and DNA repair are discussed in rela on to differen al mechanisms of defence against genotoxic damage. The paper outlines the modern concept of 'chronotherapy' -that is, an cancer therapy administered at specific mes of the day/ night cycle that could be associated with be er outcomes in some pa ents and analyses the individual variance in the tolerability of chronotherapy vs. maximum-dose an cancer therapy.Cita on: Chakarov S, Petkova R, Russev GCh, Zhelev N. DNA damage and the circadian clock.

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Time-of-day affects expression of hippocampal markers for ischemic damage induced by global ischemia

Cited by 49 publications

References 52 publications

Temporal dynamics of mouse hippocampal clock gene expression support memory processing

Temporal dynamics of mouse hippocampal clock gene expression support memory processing

Sleep Is Critical for Remote Preconditioning-Induced Neuroprotection

DNA damage and the circadian clock

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