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SUMMARY:Sleep and EEG as biological markers in animal models of Huntington
 's disease - Sandor Kantor (Department of Physiology\, Development and Neu
 roscience\, University of Cambridge)
DTSTART:20131009T113000Z
DTEND:20131009T123000Z
UID:TALK47923@talks.cam.ac.uk
CONTACT:Diane Pearce
DESCRIPTION:Summary: Although abnormal circadian rhythmicity has been demo
 nstrated in both human patients and in rodent models of Huntington's disea
 se (HD)\, a comprehensive description of sleep and electroencephalogram (E
 EG) changes has never been conducted.\n\nHere we studied sleep and EEG dis
 turbances in a transgenic mouse model of HD (R6/2 mice). We implanted EEG 
 and electromyogram electrodes into male and female R6/2 mice and their wil
 d-type (WT) littermates and then recorded baseline sleep/wake behaviour at
  pre-symptomatic\, symptomatic\, and late stages of the disease. In additi
 on\, we treated a subgroup of late stage HD mice with the tricyclic antide
 pressant amitriptyline or vehicle at dark onset\, and recorded subsequent 
 sleep/wake behaviour.\n\nWe found that sleep and EEG were already signific
 antly disrupted in R6/2 mice at the pre-symptomatic stage. The disturbance
 s worsened with age\, so that symptomatic\, R6/2 mice were unable to maint
 ain long periods of wakefulness and had an increased propensity for rapid 
 eye movement (REM) sleep. As the disease progressed\, an abnormal EEG gamm
 a activity emerged in R6/2 mice\, irrespective of sleep states. Treatment 
 with amitriptyline increased non-REM sleep amount\, reduced wake and REM s
 leep amount in both WT and R6/2 mice\, and attenuated EEG gamma activity i
 n R6/2 mice.\n\nOur results suggest that a decreased monoaminergic activit
 y may be responsible for some of the sleep and EEG symptoms found in R6/2 
 mice. If similar changes occur in humans\, these early and progressive sle
 ep and EEG abnormalities could serve as biological markers of HD.\n\nBiogr
 aphical note: Sandor joined the laboratory of Professor Jenny Morton in th
 e spring of 2011. His main interest currently is in sleep and EEG patterns
  in Huntington’s disease (HD)\, and how abnormalities in these patterns 
 might be corrected pharmacologically. He has previously worked at the Inst
 itute of Experimental Medicine of The Hungarian Academy of Sciences\, the 
 Beth Israel Deaconess Medical Center and the National Institute of Psychia
 try and Neurology in Budapest.
LOCATION:Library\, Sub-Department of Animal Behaviour\, Madingley
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