Anterior thalamic nuclei lesions and recovery of function: Relevance to cognitive thalamus |
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| Institution: | 1. New Zealand Brain Research Institute, and Department of Psychology, University of Canterbury, Christchurch 8140, New Zealand;2. Department of Medicine, University of Otago, Christchurch, New Zealand;3. School of Biological Sciences, University of Canterbury, Christchurch, New Zealand;4. Department of Psychology and Brain Health Research Centre, University of Otago, Dunedin, New Zealand;5. University of Bordeaux, INCIA, UMR 5287, F-33400 Talence, France;6. CNRS, INCIA, UMR 5287, F-33400 Talence, France;1. School of Optometry and Ophthalmology and Eye Hospital, and Key Laboratory of Visual Science, National Ministry of Health, Wenzhou Medical University, Wenzhou 325027, PR China;2. Genesys Research Institute, Tufts University, Boston, MA 02135, USA;1. University Tor Vergata, Rome, Italy;2. Laboratory of Clinical and Behavioural Neurology, IRCCS Santa Lucia Foundation, Rome, Italy;1. Department of Neurosciences and Rehabilitation, Tampere University Hospital, P.O. Box 2000, Tampere 33521, Finland;2. Department of Neurosurgery, Oulu University Hospital, P.O. Box 21, Oulu 90029, Finland;3. Medical Imaging Centre, Tampere University Hospital, P.O. Box 2000, Tampere 33521, Finland;1. Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari Aldo Moro, Bari 70124, Italy;2. Toulouse NeuroImaging Center, Université de Toulouse, Inserm, UPS 31024, France;3. CHU Toulouse Purpan, Neurology Department, Toulouse 31059, France;4. Normandie University, UNICAEN, PSL Research University, EPHE, INSERM, U1077, CHU de Caen, Neuropsychologie et Imagerie de la Mémoire Humaine, 14000 Caen, France;5. Department of Systems Medicine, Tor Vergata University and S. Lucia Foundation, Rome, Italy;6. Clinical Neuropsychology, Ruhr University Bochum, Universitätsstrasse 150, 44801 Bochum, Germany;7. Department of Experimental Psychology, University of Oxford, The Tinsley Building, Mansfield Road, Oxford OX1 3SR, UK;8. Centre de recherche Cerveau et Cognition, UMR5549, Université de Toulouse – CNRS, Toulouse 31000, France;9. Equivalent contribution as last authors |
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| Abstract: | Injury to the anterior thalamic nuclei (ATN) and their neural connections is the most consistent neuropathology associated with diencephalic amnesia. ATN lesions in rats produce memory impairments that support a key role for this region within an extended hippocampal system of complex overlapping neural connections. Environmental enrichment is a therapeutic tool that produces substantial, although incomplete, recovery of memory function after ATN lesions, even after the lesion-induced deficit has become established. Similarly, the neurotrophic agent cerebrolysin, also counters the negative effects of ATN lesions. ATN lesions substantially reduce c-Fos expression and spine density in the retrosplenial cortex, and reduce spine density on CA1 neurons; only the latter is reversed by enrichment. We discuss the implications of this evidence for the cognitive thalamus, with a proposal that there are genuine interactions among different but allied thalamo-cortical systems that go beyond a simple summation of their separate effects. |
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| Keywords: | Thalamic amnesia Enrichment Spines Retrosplenial CA1 Cerebrolysin |
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