Circadian rhythm. Dysrhythmia in the suprachiasmatic nucleus inhibits memory processing.
Chronic circadian dysfunction impairs declarative memory in humans but has little effect in common rodent models of arrhythmia caused by clock gene knockouts or surgical ablation of the suprachiasmatic nucleus (SCN). An important problem overlooked in these translational models is that human dysrhythmia occurs while SCN circuitry is genetically and neurologically intact. Siberian hamsters (Phodopus sungorus) are particularly well suited for translational studies because they can be made arrhythmic by a one-time photic treatment that severely impairs spatial and recognition memory. We found that once animals are made arrhythmic, subsequent SCN ablation completely rescues memory processing. These data suggest that the inhibitory effects of a malfunctioning SCN on cognition require preservation of circuitry between the SCN and downstream targets that are lost when these connections are severed.
Department of Psychiatry and Behavioral Sciences, Stanford University, Palo Alto, CA, USA.
Fabian
F
Fernandez
Biology Department, Stanford University, Stanford CA, USA.
Derek
D
Lu
Biology Department, Stanford University, Stanford CA, USA.
Phong
P
Ha
Biology Department, Stanford University, Stanford CA, USA.
Patricia
P
Costacurta
Biology Department, Stanford University, Stanford CA, USA.
Renee
R
Chavez
Biology Department, Stanford University, Stanford CA, USA.
H Craig
HC
Heller
Biology Department, Stanford University, Stanford CA, USA. ruby@stanford.edu.
Norman F
NF
Ruby
D000818:Animals; D002940:Circadian Rhythm; D006224:Cricetinae; D006801:Humans; D008569:Memory Disorders / Q000503:physiopathology*; D017111:Phodopus; D010775:Photic Stimulation; D021641:Recognition, Psychology / Q000502:physiology*; D065852:Spatial Memory / Q000502:physiology*; D013493:Suprachiasmatic Nucleus / Q000503:physiopathology*