Chronic nicotine intake decelerates aging of nigrostriatal dopaminergic neurons

Life Sci. 1994;54(16):1169-84. doi: 10.1016/0024-3205(94)00839-6.

Abstract

We have evaluated the effect of chronic nicotine intake on the age-associated loss of nigrostriatal dopaminergic neurons. The striatal density of dopamine (D1 and D2) receptors and DA-uptake sites decreased with age. Concomitant with these changes was a pronounced loss of many behavioral functions associated, at least in part, with dopaminergic neurotransmission. Chronic oral intake of nicotine resulted in partial restoration of the loss of receptors as well as behavioral performances. The results suggest that low doses of nicotine could have beneficial effects during aging.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / metabolism
  • Animals
  • Apomorphine / pharmacology
  • Benzazepines / metabolism
  • Binding Sites
  • Body Weight / drug effects
  • Cellular Senescence / drug effects
  • Corpus Striatum / cytology
  • Corpus Striatum / drug effects*
  • Corpus Striatum / metabolism
  • Domperidone / metabolism
  • Dopamine / metabolism
  • Male
  • Mazindol / metabolism
  • Neurons / drug effects*
  • Neurons / metabolism
  • Nicotine / administration & dosage
  • Nicotine / pharmacology*
  • Rats
  • Rats, Inbred F344
  • Receptors, Dopamine D1 / metabolism
  • Receptors, Dopamine D2 / metabolism
  • Substantia Nigra / cytology
  • Substantia Nigra / drug effects*
  • Substantia Nigra / metabolism

Substances

  • Benzazepines
  • Receptors, Dopamine D1
  • Receptors, Dopamine D2
  • Domperidone
  • Nicotine
  • Mazindol
  • Apomorphine
  • Dopamine