Genetically dystrophic mdx/mdx mice exhibit decreased response to nicotine in passive avoidance

Roberto Coccurello, Claudio Castellano, Paola Paggi, Andrea Mele, Alberto Oliverio

Research output: Contribution to journalArticlepeer-review


mdx mice are considered as a genetic homologous of human Duchenne muscular dystrophy. Recent evidence demonstrates that in mouse sympathetic ganglion dystrophin is involved in the stabilization of nicotinic acetylcholine receptor clusters. The purpose of this study was to verify possible effects of dystrophin alterations at the central level. This was assessed by evaluating the response to nicotine administration in mdx and wild-type mice. Thus the effects of post-training nicotine administrations (0.1, 0.25 and 0.5 mg/kg) were tested in mice subjected to a passive avoidance memory task, that measures the ability of mice to remember on test day a shock received 24 h before. Nicotine enhanced memory in wild-type as well as in mdx mice. However, the doses needed to increase memory in mdx were higher than in wild-type. These results are discussed in terms of possible functional changes in central nicotinic acetylcholine receptor in mdx mice.

Original languageEnglish
Pages (from-to)1219-1222
Number of pages4
Issue number9
Publication statusPublished - Jul 2 2002


  • Acetylcholine receptor imbalance
  • Duchenne muscular dystrophy
  • Mdx mice
  • Memory consolidation
  • Nicotine

ASJC Scopus subject areas

  • Neuroscience(all)


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