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Abstract
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.
The Sun rises (and sets) on hamster memories
Internal circadian clocks set a rhythm to which biological systems beat. In addition to regulating sleep and wake cycles, the circadian system influences learning and memory. Using Siberian hamsters as a model, Fernandez et al. evaluated the role of the part of the brain that regulates the circadian cycle, the suprachiasmatic nucleus (SCN), in altered memory processing when circadian rhythms are disrupted. As expected, animals with disrupted rhythms had recognition and spatial memory impairments. However, when the animals' SCN was disconnected, these memory deficits were reversed. Thus, memory impairment resulting from circadian dysfunction is dependent on preserving SCN circuit connections.
Science, this issue p. 854
