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Circadian Regulation of Synaptic Plasticity

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.


Central and peripheral clocks influence synaptic plasticity. Central clocks like the mammalian suprachiasmatic nucleus (SCN) can impose rhythms in non-clock circuits via several mechanisms. These include rhythms in hormonse and neuromodulator output (e.g., cycles of glucocorticoid release from the adrenal glands) which can alter synapses widely throughout the brain. The SCN also directly drives rhythms in core and brain temperature. Temperature profoundly influences neural function and synaptic plasticity. Temperature may also operate to entrain peripheral clocks in non-SCN neurons. Peripheral clocks themselves can direct plastic changes due to the expression of cannonical clock genes outside central clocks.
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biology-05-00031-f001: Central and peripheral clocks influence synaptic plasticity. Central clocks like the mammalian suprachiasmatic nucleus (SCN) can impose rhythms in non-clock circuits via several mechanisms. These include rhythms in hormonse and neuromodulator output (e.g., cycles of glucocorticoid release from the adrenal glands) which can alter synapses widely throughout the brain. The SCN also directly drives rhythms in core and brain temperature. Temperature profoundly influences neural function and synaptic plasticity. Temperature may also operate to entrain peripheral clocks in non-SCN neurons. Peripheral clocks themselves can direct plastic changes due to the expression of cannonical clock genes outside central clocks.

Mentions: Circadian regulation of synaptic plasticity can involve central or peripheral clocks (Figure 1). Central clocks refer to dedicated cells or nuclei that impose rhythmicity on target structures. The mammalian SCN is one example. Peripheral clocks refer to oscillators that express canonical clock genes, are often synchronized by central clocks, but can operate independently from central clocks [46,47]. An example is the peripheral clock in the Drosophila MN5 motor neuron. Central clocks can influence plasticity in three ways. These are the production of 24-h rhythms in brain temperature, hormone and neuromodulator release and GABAergic inhibition. Peripheral clocks may influence plasticity via signaling pathways downstream of cycling clock genes. I discuss these topics below.


Circadian Regulation of Synaptic Plasticity
Central and peripheral clocks influence synaptic plasticity. Central clocks like the mammalian suprachiasmatic nucleus (SCN) can impose rhythms in non-clock circuits via several mechanisms. These include rhythms in hormonse and neuromodulator output (e.g., cycles of glucocorticoid release from the adrenal glands) which can alter synapses widely throughout the brain. The SCN also directly drives rhythms in core and brain temperature. Temperature profoundly influences neural function and synaptic plasticity. Temperature may also operate to entrain peripheral clocks in non-SCN neurons. Peripheral clocks themselves can direct plastic changes due to the expression of cannonical clock genes outside central clocks.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5037350&req=5

biology-05-00031-f001: Central and peripheral clocks influence synaptic plasticity. Central clocks like the mammalian suprachiasmatic nucleus (SCN) can impose rhythms in non-clock circuits via several mechanisms. These include rhythms in hormonse and neuromodulator output (e.g., cycles of glucocorticoid release from the adrenal glands) which can alter synapses widely throughout the brain. The SCN also directly drives rhythms in core and brain temperature. Temperature profoundly influences neural function and synaptic plasticity. Temperature may also operate to entrain peripheral clocks in non-SCN neurons. Peripheral clocks themselves can direct plastic changes due to the expression of cannonical clock genes outside central clocks.
Mentions: Circadian regulation of synaptic plasticity can involve central or peripheral clocks (Figure 1). Central clocks refer to dedicated cells or nuclei that impose rhythmicity on target structures. The mammalian SCN is one example. Peripheral clocks refer to oscillators that express canonical clock genes, are often synchronized by central clocks, but can operate independently from central clocks [46,47]. An example is the peripheral clock in the Drosophila MN5 motor neuron. Central clocks can influence plasticity in three ways. These are the production of 24-h rhythms in brain temperature, hormone and neuromodulator release and GABAergic inhibition. Peripheral clocks may influence plasticity via signaling pathways downstream of cycling clock genes. I discuss these topics below.

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.