Network Dynamics Mediate Circadian Clock Plasticity. Neuron 2017 Jan 18;93(2):441-450
Date
01/10/2017Pubmed ID
28065650Pubmed Central ID
PMC5247339DOI
10.1016/j.neuron.2016.12.022Scopus ID
2-s2.0-85008485774 (requires institutional sign-in at Scopus site) 50 CitationsAbstract
A circadian clock governs most aspects of mammalian behavior. Although its properties are in part genetically determined, altered light-dark environment can change circadian period length through a mechanism requiring de novo DNA methylation. We show here that this mechanism is mediated not via cell-autonomous clock properties, but rather through altered networking within the suprachiasmatic nuclei (SCN), the circadian "master clock," which is DNA methylated in region-specific manner. DNA methylation is necessary to temporally reorganize circadian phasing among SCN neurons, which in turn changes the period length of the network as a whole. Interruption of neural communication by inhibiting neuronal firing or by physical cutting suppresses both SCN reorganization and period changes. Mathematical modeling suggests, and experiments confirm, that this SCN reorganization depends upon GABAergic signaling. Our results therefore show that basic circadian clock properties are governed by dynamic interactions among SCN neurons, with neuroadaptations in network function driven by the environment.
Author List
Azzi A, Evans JA, Leise T, Myung J, Takumi T, Davidson AJ, Brown SAAuthor
Jennifer A. Evans PhD Assistant Professor in the Biomedical Sciences department at Marquette UniversityMESH terms used to index this publication - Major topics in bold
Action PotentialsAnimals
Circadian Clocks
Circadian Rhythm
DNA Methylation
Light
Male
Mice
Models, Theoretical
Neurons
Patch-Clamp Techniques
Period Circadian Proteins
Suprachiasmatic Nucleus
Thalamus
gamma-Aminobutyric Acid
