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Keywords:

  • Nicotine;
  • Striatum;
  • Methionine-enkephalin;
  • Preproenkephalin mRNA;
  • Mecamylamine;
  • Nicotinic receptors

Abstract: A single dose of nicotine increased methionine-enkephalin (Met-Enk) immunoreactivity in the striatum of mice in a time-dependent manner. Met-Enk content reached a maximum by ∼1 h after nicotine and returned to control values by 6 h. The response to nicotine was blocked by pretreating animals with the nicotinic receptor antagonist mecamylamine. In contrast, pretreating mice with the muscarinic receptor antagonist atropine or the dopamine receptor antagonist haloperidol did not block the response. A single dose of nicotine also increased mRNA for the precursor peptide preproenkephalin (PPE). The increase of PPE mRNA preceded that of Met-Enk and reached a maximum by ∼30 min after nicotine. PPE mRNA levels returned to near normal by ∼3 h and increased again by 6 h after nicotine. Daily administration of nicotine for 14 days increased Met-Enk content and PPE mRNA in the striatum of mice as well. Taken together, our results suggest that nicotinic receptors modulate Met-Enk content and PPE mRNA in the mouse striatum.