4.3 Article

Exploratory, anxiety and spatial memory impairments are dissociated in mice lacking the LPA1 receptor

期刊

NEUROBIOLOGY OF LEARNING AND MEMORY
卷 94, 期 1, 页码 73-82

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nlm.2010.04.003

关键词

Lysophosphatidic acid; Knockout mice; Hole-board; Principal components factorial analysis; Spatial reference memory; Spatial working memory; Habituation

资金

  1. Human Frontier Science Programme
  2. MEC [SEJ2007-61187]
  3. I3SNS Programme
  4. FIS [02/1643, PI07/0629]
  5. Red CIEN [G03/06]
  6. Instituto de Salud Carlos III, Spanish Ministry of Health and Andalusian Ministries of Health and of Innovation, Science and Enterprise [CTS065, CTS433]
  7. National Institutes of Health (USA) [MH51699, MH01723]
  8. Spanish Ministry of Education [AP-2006-02582, AP-2007-03719]

向作者/读者索取更多资源

Lysophosphatidic acid (LPA) is a new, intercellular signalling molecule in the brain that has an important role in adult hippocampal plasticity. Mice lacking the LPA, receptor exhibit motor, emotional and cognitive alterations. However, the potential relationship among these concomitant impairments was unclear. Wild-type and maLPA(1)-null mice were tested on the hole-board for habituation and spatial learning. MaLPA(1)-null mice exhibited reduced exploration in a novel context and a defective intersession habituation that also revealed increased anxiety-like behaviour throughout the hole-board testing. In regard to spatial memory, maLPA(1) nulls failed to reach the controls' performance at the end of the reference memory task. Moreover, their defective working memory on the first training day suggested a delayed acquisition of the task's working memory rule, which is also a long term memory component. The temporal interval between trials and the task's difficulty may explain some of the deficits found in these mice. Principal components analysis revealed that alterations found in each behavioural dimension were independent. Therefore, exploratory and emotional impairments did not account for the cognitive deficits that may be attributed to maLPA(1) nulls' hippocampal malfunction. (c) 2010 Elsevier Inc. All rights reserved.

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