Lesions of the anterior thalamic nuclei and intralaminar thalamic nuclei: place and visual discrimination learning in the water maze |
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Authors: | Pierre-Henri Moreau Yanina Tsenkina Lucas Lecourtier Joëlle Lopez Brigitte Cosquer Mathieu Wolff John Dalrymple-Alford Jean-Christophe Cassel |
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Affiliation: | 1. Laboratoire d’Imagerie et Neurosciences Cognitives, UMR 7237, Université de Strasbourg, CNRS, IFR 37 Neurosciences, GDR CNRS 2905, 12 Rue Goethe, 67000, Strasbourg, France 2. University of Bordeaux, INCIA, UMR 5287, 33400, Talence, France 3. CNRS, INCIA, UMR 5287, 33400, Talence, France 4. New Zealand Brain Research Institute, Christchurch, 8011, New Zealand 5. Department of Psychology, University of Canterbury, Christchurch, 8140, New Zealand 6. Department of Medicine, University of Otago, Christchurch, New Zealand
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Abstract: | Medial thalamic damage produces memory deficits in humans (e.g., Korsakoff’s syndrome) and experimental animals. Both the anterior thalamic nuclei (ATN) and rostral intralaminar plus adjacent lateral thalamic nuclei (ILN/LT) have been implicated. Based on the differences in their main connections with other neural structures, we tested the prediction that ATN lesions would selectively impair acquisition of spatial location discrimination, reflecting a hippocampal system deficit, whereas ILN/LT lesions would impair acquisition of visual pattern discrimination, reflecting a striatal system deficit. Half the rats were first trained in a spatial task in a water maze before switching to a visual task in the same maze, while the remainder were tested with the reverse order of tasks. Compared with sham-operated controls, (1) rats with ATN lesions showed impaired place learning, but normal visual discrimination learning, (2) rats with ILN/LT lesions showed no deficit on either task. Rats with ATN lesions were also hyperactive when their home cage was placed in a novel room and remained more active than ILN/LT or SHAM rats for the subsequent 21 h, especially during the nocturnal phase. These findings confirmed the influence of ATN lesions on spatial learning, but failed to support the view that ILN/LT lesions disrupt striatal-dependent memory. |
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