Savings and extinction of conditioned eyeblink responses in fragile X syndrome

Genes Brain Behav. 2008 Oct;7(7):770-7. doi: 10.1111/j.1601-183X.2008.00417.x. Epub 2008 Jun 30.


The fragile X syndrome (FRAXA) is the most widespread heritable form of mental retardation caused by the lack of expression of the fragile X mental retardation protein (FMRP). This lack has been related to deficits in cerebellum-mediated acquisition of conditioned eyelid responses in individuals with FRAXA. In the present behavioral study, long-term effects of deficiency of FMRP were investigated by examining the acquisition, savings and extinction of delay eyeblink conditioning in male individuals with FRAXA. In the acquisition experiment, subjects with FRAXA displayed a significantly poor performance compared with controls. In the savings experiment performed at least 6 months later, subjects with FRAXA and controls showed similar levels of savings of conditioned responses. Subsequently, extinction was faster in subjects with FRAXA than in controls. These findings confirm that absence of the FMRP affects cerebellar motor learning. The normal performance in the savings experiment and aberrant performance in the acquisition and extinction experiments of individuals with FRAXA suggest that different mechanisms underlie acquisition, savings and extinction of cerebellar motor learning.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cerebellum / pathology
  • Cerebellum / physiopathology
  • Conditioning, Eyelid / physiology*
  • Data Interpretation, Statistical
  • Extinction, Psychological / physiology*
  • Female
  • Fragile X Mental Retardation Protein / genetics
  • Fragile X Mental Retardation Protein / physiology
  • Fragile X Syndrome / genetics*
  • Fragile X Syndrome / pathology*
  • Fragile X Syndrome / psychology
  • Humans
  • Intelligence Tests
  • Learning / physiology
  • Male
  • Middle Aged
  • Motor Skills
  • Young Adult


  • Fragile X Mental Retardation Protein