Dysrhythmia in the suprachiasmatic nucleus inhibits memory processing

Fabian Fernandez, Derek Lu, Phong Ha, Patricia Costacurta, Renee Chavez, H. Craig Heller, Norman F. Ruby

Research output: Contribution to journalArticlepeer-review

82 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)854-857
Number of pages4
Issue number6211
StatePublished - Nov 14 2014
Externally publishedYes

ASJC Scopus subject areas

  • General


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