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The Journal of Neuroscience, March 23, 2005, 25(12):3059-3066; doi:10.1523/JNEUROSCI.4320-04.2005

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Behavioral/Systems/Cognitive
Deficits in Experience-Dependent Cortical Plasticity and Sensory-Discrimination Learning in Presymptomatic Huntington's Disease Mice

Nektarios K. Mazarakis,¹ Anita Cybulska-Klosowicz,² Helen Grote,¹ Terence Pang,³ Anton Van Dellen,¹ Malgorzata Kossut,¹ Colin Blakemore,¹ and Anthony J. Hannan^1,3

¹University Laboratory of Physiology, University of Oxford, Oxford OX1 3PT, United Kingdom, ²Laboratory of Cortical Plasticity, Nencki Institute of Experimental Biology, 02-093 Warsaw, Poland, and ³Howard Florey Institute, University of Melbourne, Parkville, 3010 Victoria, Australia

Huntington's disease (HD) is one of a group of neurodegenerative diseases caused by an expanded trinucleotide (CAG) repeat coding for an extended polyglutamine tract. The disease is inherited in an autosomal dominant manner, with onset of motor, cognitive, and psychiatric symptoms typically occurring in midlife, followed by unremitting progression and eventual death. We report here that motor presymptomatic R6/1 HD mice show a severe impairment of somatosensory-discrimination learning ability in a behavioral task that depends heavily on the barrel cortex. In parallel, there are deficits in barrel-cortex plasticity after a somatosensory whisker-deprivation paradigm. The present study demonstrates deficits in neocortical plasticity correlated with a specific learning impairment involving the same neocortical area, a finding that provides new insight into the cellular basis of early cognitive deficits in HD.

Key words: Huntington's disease; barrel; plasticity; whiskers; learning; cortex

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Received Dec 6, 2003; revised February 1, 2005; accepted February 1, 2005.

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