Continuous reversal using internal or external cues: A novel test measuring set shifting in Parkinsonian rats
| Autor: | Süleyman Kaplan, Yasin Temel, Thibaut Sesia, Rinske Vlamings, Eva Wolbert, Arjan Blokland, Rob Hameleers |
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| Přispěvatelé: | Ondokuz Mayıs Üniversitesi |
| Rok vydání: | 2012 |
| Předmět: |
Lever
business.product_category Parkinson's disease Tyrosine hydroxylase business.industry Bradyphrenia Cognitive flexibility Cognition General Medicine medicine.disease Set-shifting Continuous reversal 6-OHDA lesion Parkinson’s disease General Biochemistry Genetics and Molecular Biology Task (project management) 6-OHDA lesion Set-shifting Lesion Health Care Sciences and Services medicine Continuous reversal Sağlık Bilimleri ve Hizmetleri medicine.symptom business Neuroscience psychological phenomena and processes |
| Zdroj: | Volume: 29, Issue: 3 183-186 Journal of Experimental and Clinical Medicine |
| ISSN: | 1309-5129 1309-4483 |
| DOI: | 10.5835/jecm.omu.29.03.005 |
| Popis: | Parkinson’s disease (PD) is a predominant movement disorder, but profound cognitive deficits (e.g. bradyphrenia, memory, and set shifting) also occur. To model the deficits in set shifting using internal and external cues in rats we developed a continuous reversal task in which the active lever, left or right lever, alternated after a variable number of lever presses. In one task the active lever was signaled by a light (external cue condition, EC) whereas in the other task the active lever was not signaled (internal cue condition, IC). In this study we evaluated the effects of a partial bilateral striatal 6-OHDA lesion as model for PD on the performance in both tasks. Following behavioral testing the lesions were verified using tyrosine hydroxylase (TH) immunohistochemistry. The 6-OHDA lesioned animals were specifically impaired in the IC condition and not in the EC task. In other words, the lesioned animals kept pressing a lever longer although it was not longer active. The present response switching task is sensitive to 6-OHDA lesions and may mimic set-shifting deficits in PD. J. Exp. Clin. Med., 2012; 29:183-186 |
| Databáze: | OpenAIRE |
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