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Circadian Regulation of Synaptic Plasticity

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ABSTRACT

Circadian rhythms refer to oscillations in biological processes with a period of approximately 24 h. In addition to the sleep/wake cycle, there are circadian rhythms in metabolism, body temperature, hormone output, organ function and gene expression. There is also evidence of circadian rhythms in synaptic plasticity, in some cases driven by a master central clock and in other cases by peripheral clocks. In this article, I review the evidence for circadian influences on synaptic plasticity. I also discuss ways to disentangle the effects of brain state and rhythms on synaptic plasticity.

No MeSH data available.


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A State-Clock Model (SCM) of sleep and circadian regulation of synaptic plasticity. According to the SCM, biological clocks produce circuit-specific, 24-h rhythms in synaptic efficacy and morphology. It proposes that global synaptic changes observed across sleep and wake are driven by clocks and not brain state. This ensures that an organism’s nervous system is optimized to encode experience during wakefulness and separates the induction and consolidation of plastic changes across the 24-h day. The latter process would then be expected to coincide with brain states conducive for consolidation (sleep). HPA = Hypothalamic-Pituitary-Adrenal axis.
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biology-05-00031-f002: A State-Clock Model (SCM) of sleep and circadian regulation of synaptic plasticity. According to the SCM, biological clocks produce circuit-specific, 24-h rhythms in synaptic efficacy and morphology. It proposes that global synaptic changes observed across sleep and wake are driven by clocks and not brain state. This ensures that an organism’s nervous system is optimized to encode experience during wakefulness and separates the induction and consolidation of plastic changes across the 24-h day. The latter process would then be expected to coincide with brain states conducive for consolidation (sleep). HPA = Hypothalamic-Pituitary-Adrenal axis.

Mentions: Based on these and similar observations, a “State-Clock” model (SCM) was proposed (Figure 2), according to which outputs of the biological clock produce circuit-specific, 24-h rhythms in synaptic efficacy and morphology [4]. In contrast to other theories [78], it proposes that global synaptic changes observed across sleep and wake are driven by clocks and not brain state. The SCM thus may account for some of the variability in synaptic changes reported after sleep. For example, it explains why evidence of global synaptic weakening after sleep is not reported in carnivores with weak or absent circadian organization [4]. It also accounts for the observation that evidence of global synaptic weakening in rodents in vivo is typically reported when measurements are made after long periods of sleep (e.g., 6 or 12 h) [5]. However, when conducted this way, measurements made before and after sleep occur at very different phases of the circadian cycle.


Circadian Regulation of Synaptic Plasticity
A State-Clock Model (SCM) of sleep and circadian regulation of synaptic plasticity. According to the SCM, biological clocks produce circuit-specific, 24-h rhythms in synaptic efficacy and morphology. It proposes that global synaptic changes observed across sleep and wake are driven by clocks and not brain state. This ensures that an organism’s nervous system is optimized to encode experience during wakefulness and separates the induction and consolidation of plastic changes across the 24-h day. The latter process would then be expected to coincide with brain states conducive for consolidation (sleep). HPA = Hypothalamic-Pituitary-Adrenal axis.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037350&req=5

biology-05-00031-f002: A State-Clock Model (SCM) of sleep and circadian regulation of synaptic plasticity. According to the SCM, biological clocks produce circuit-specific, 24-h rhythms in synaptic efficacy and morphology. It proposes that global synaptic changes observed across sleep and wake are driven by clocks and not brain state. This ensures that an organism’s nervous system is optimized to encode experience during wakefulness and separates the induction and consolidation of plastic changes across the 24-h day. The latter process would then be expected to coincide with brain states conducive for consolidation (sleep). HPA = Hypothalamic-Pituitary-Adrenal axis.
Mentions: Based on these and similar observations, a “State-Clock” model (SCM) was proposed (Figure 2), according to which outputs of the biological clock produce circuit-specific, 24-h rhythms in synaptic efficacy and morphology [4]. In contrast to other theories [78], it proposes that global synaptic changes observed across sleep and wake are driven by clocks and not brain state. The SCM thus may account for some of the variability in synaptic changes reported after sleep. For example, it explains why evidence of global synaptic weakening after sleep is not reported in carnivores with weak or absent circadian organization [4]. It also accounts for the observation that evidence of global synaptic weakening in rodents in vivo is typically reported when measurements are made after long periods of sleep (e.g., 6 or 12 h) [5]. However, when conducted this way, measurements made before and after sleep occur at very different phases of the circadian cycle.

View Article: PubMed Central - PubMed

ABSTRACT

Circadian rhythms refer to oscillations in biological processes with a period of approximately 24 h. In addition to the sleep/wake cycle, there are circadian rhythms in metabolism, body temperature, hormone output, organ function and gene expression. There is also evidence of circadian rhythms in synaptic plasticity, in some cases driven by a master central clock and in other cases by peripheral clocks. In this article, I review the evidence for circadian influences on synaptic plasticity. I also discuss ways to disentangle the effects of brain state and rhythms on synaptic plasticity.

No MeSH data available.


Related in: MedlinePlus