RT Journal Article
SR Electronic
T1 Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 5891
OP 5899
DO 10.1523/JNEUROSCI.0469-12.2012
VO 32
IS 17
A1 Sahar Farajnia
A1 Stephan Michel
A1 Tom Deboer
A1 Henk Tjebbe vanderLeest
A1 Thijs Houben
A1 Jos H. T. Rohling
A1 Ashna Ramkisoensing
A1 Roman Yasenkov
A1 Johanna H. Meijer
YR 2012
UL http://www.jneurosci.org/content/32/17/5891.abstract
AB Aging is associated with a deterioration of daily (circadian) rhythms in physiology and behavior. Deficits in the function of the central circadian pacemaker in the suprachiasmatic nucleus (SCN) have been implicated, but the responsible mechanisms have not been clearly delineated. In this report, we characterize the progression of rhythm deterioration in mice to 900 d of age. Longitudinal behavioral and sleep–wake recordings in up to 30-month-old mice showed strong fragmentation of rhythms, starting at the age of 700 d. Patch-clamp recordings in this age group revealed deficits in membrane properties and GABAergic postsynaptic current amplitude. A selective loss of circadian modulation of fast delayed-rectifier and A-type K+ currents was observed. At the tissue level, phase synchrony of SCN neurons was grossly disturbed, with some subpopulations peaking in anti-phase and a reduction in amplitude of the overall multiunit activity rhythm. We propose that aberrant SCN rhythmicity in old animals—with electrophysiological arrhythmia at the single-cell level and phase desynchronization at the network level—can account for defective circadian function with aging.