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Tytuł pozycji:

Early cognitive dysfunction in the HD 51 CAG transgenic rat model of Huntington's disease.

Tytuł:
Early cognitive dysfunction in the HD 51 CAG transgenic rat model of Huntington's disease.
Autorzy:
Fink KD; Program in Neuroscience, Central Michigan University, USA.
Rossignol J
Crane AT
Davis KK
Bavar AM
Dekorver NW
Lowrance SA
Reilly MP
Sandstrom MI
von Hörsten S
Lescaudron L
Dunbar GL
Źródło:
Behavioral neuroscience [Behav Neurosci] 2012 Jun; Vol. 126 (3), pp. 479-87.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: Washington, D.C. : American Psychological Association, [c1983-
MeSH Terms:
Cognition Disorders/*genetics
Huntington Disease/*genetics
Nerve Tissue Proteins/*genetics
Trinucleotide Repeats/*genetics
Animals ; Cell Death/genetics ; Cognition Disorders/psychology ; Conditioning, Operant/physiology ; Disease Models, Animal ; Humans ; Huntingtin Protein ; Huntington Disease/pathology ; Huntington Disease/psychology ; Male ; Random Allocation ; Rats ; Rats, Transgenic
Substance Nomenclature:
0 (HTT protein, human)
0 (Huntingtin Protein)
0 (Nerve Tissue Proteins)
Entry Date(s):
Date Created: 20120531 Date Completed: 20130325 Latest Revision: 20161125
Update Code:
20240104
DOI:
10.1037/a0028028
PMID:
22642889
Czasopismo naukowe
Huntington's disease (HD) is a neurodegenerative disorder in humans caused by an expansion of a CAG trinucleotide repeat that produces choreic movements, which are preceded by cognitive deficits. The HD transgenic rat (tgHD), which contains the human HD mutation with a 51 CAG repeat allele, exhibits motor deficits that begin when these rats are 12 months of age. However, there are no reports of cognitive dysfunction occurring prior to this. To assess whether cognitive dysfunction might precede motor deficits in tgHD rats, one group of 9-month-old male rats with homozygotic mutated genes and one group of wild-type (WT) rats underwent three testing phases in a unique Spatial Operant Reversal Test (SORT) paradigm, as well as assessment of spontaneous motor activity. After testing, morphological and histological examination of the brains were made. Results indicated that tgHD rats acquired the cued-response (Phase 1) portion of the SORT, but made significantly more errors during the reversal (Phase 2) and during the pseudorandomized reversals (Phase 3) portion of the study, when compared to WT rats. Analysis of the data using mathematical principles of reinforcement revealed no memory, motor, or motivational deficits. These results indicate that early cognitive dysfunction, as measured by the SORT, occur prior to motor deficits, gross anatomical changes, or cell loss in the tgHD rat with 51 CAG repeats, and suggest that this protocol could provide a useful screen for therapeutic studies.
(© 2012 American Psychological Association)

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