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.
Highlights
Synaptic plasticity can be defined as changes in the strength of existing synapses, changes in synapse number or size, or changes in morphological structures that contain or form synapses
The roles of experience and development are increasingly well understood, but the precise role of sleep remains mysterious. This is because the effects of sleep on synaptic plasticity vary across species, brain region and ontogenetic status and are partly determined by the kinds of experience that precede sleep [4]
Deletion of canonical clock genes (Per1 and Bmal) reduces the magnitude of hippocampal LTP in situ [15,16,17]. These findings indicate that peripheral clocks regulate plasticity in the hippocampus
Summary
Synaptic plasticity can be defined as changes in the strength of existing synapses, changes in synapse number or size, or changes in morphological structures that contain or form synapses (e.g., dendritic spines and synaptic boutons). Three physiological factors are recognized to trigger or influence synaptic plasticity in vivo: Waking experience, developmental programs and sleep (neurodegenerative synaptic changes are not included as they reflect pathological processes). The roles of experience and development are increasingly well understood, but the precise role of sleep remains mysterious This is because the effects of sleep on synaptic plasticity vary across species, brain region and ontogenetic status and are partly determined by the kinds of experience that precede sleep [4]. This article extends and further develops topics I have discussed elsewhere [4] This includes a more detailed investigation of how circadian processes can alter synapse number or strength [4] (for a discussion of clock mechanisms themselves, see [9])
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