Nicotine imptoves cognitive disturbance in senescence-accelerated mice

K. Meguro, S. Yamaguchi, H. Arai, T. Nakagawa, C. Doi, M. Yamada, Y. Ikarashi, Y. Maruyama, H. Sasaki

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)


Senescence-accelerated mice (SAM), a murine model of age-related deterioration in learning ability, were studied as to the acetylcholine (ACh) contents in the brain tissues and the effect of nicotine administration. We found that the ACh content of SAM-P/8 (accelerated senescence-prone) mice was lower than that of SAM-R/1 (accelerated senescence-resistant) mice in the midbrain thalamus and the hypothalamus. In addition, an IP administration of nicotine was found to improve learning ability of SAM-P/8 as shown by performance of a passive avoidance task. Nicotine may potentiate cognitive function in SAM-P/8.

Original languageEnglish
Pages (from-to)769-772
Number of pages4
JournalPharmacology, Biochemistry and Behavior
Issue number3
Publication statusPublished - 1994 Nov
Externally publishedYes


  • Acetylcholine
  • Alzheimer's disease
  • Nicotine
  • Senescence-accelerated mice (SAM)
  • Tobacco

ASJC Scopus subject areas

  • Biochemistry
  • Toxicology
  • Pharmacology
  • Clinical Biochemistry
  • Biological Psychiatry
  • Behavioral Neuroscience


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