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Why do lesions in the rodent anterior thalamic nuclei cause such severe spatial deficits?

期刊

NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
卷 54, 期 -, 页码 131-144

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neubiorev.2014.08.013

关键词

Alternation; Amnesia; Direction; Fornix; Learning; Mammillary bodies; Memory; Navigation; Space; Thalamus

资金

  1. Biotechnology and Biological Sciences Research Council [BB/H020187/1] Funding Source: researchfish
  2. Wellcome Trust [103722/Z/14/Z] Funding Source: researchfish
  3. Wellcome Trust [103722/Z/14/Z] Funding Source: Wellcome Trust
  4. BBSRC [BB/H020187/1] Funding Source: UKRI
  5. Biotechnology and Biological Sciences Research Council [BB/H020187/1] Funding Source: Medline
  6. Wellcome Trust [103722, WT092480] Funding Source: Medline

向作者/读者索取更多资源

Lesions of the rodent anterior thalamic nuclei cause severe deficits to multiple spatial learning tasks. Possible explanations for these effects are examined, with particular reference to T-maze alternation. Anterior thalamic lesions not only impair allocentric place learning but also disrupt other spatial processes, including direction learning, path integration, and relative length discriminations, as well as aspects of nonspatial learning, e.g., temporal discriminations. Working memory tasks, such as T-maze alternation, appear particularly sensitive as they combine an array of these spatial and nonspatial demands. This sensitivity partly reflects the different functions supported by individual anterior thalamic nuclei, though it is argued that anterior thalamic lesion effects also arise from covert pathology in sites distal to the thalamus, most critically in the retrosplenial cortex and hippocampus. This two-level account, involving both local and distal lesion effects, explains the range and severity of the spatial deficits following anterior thalamic lesions. These findings highlight how the anterior thalamic nuclei form a key component in a series of interdependent systems that support multiple spatial functions. (c) 2014 The Authors. Published by Elsevier Ltd.

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