Chapter 18 Nicotine and opioid peptides

Abstract

This chapter discusses the relationship between nicotinic cholinergic receptors and opioid peptides. Nicotine appears to exert its stimulatory effect most likely at the level of the hypothalamus by causing a release of corticotropin releasing factor. In contrast to the acute treatment, normal levels of ACTH and/or glucocorticoids have been observed after chronic administration of nicotineindicating that tolerance to the stimulatory effect of nicotine on the hypothalamo-pituitary-adrenal axis can develop. Moreover, chronic administration of nicotine into mice did not change the levels of immunoreactive β -endorphin in the pituitary. The chapter investigated the effect of chronic nicotine treatment on the levels of β -endorphin, Met-enkephalin and other neuropeptides in various areas of the mouse brain. With the exception of the levels of β -endorphin in the hypothalamus, no significant changes in the brain concentrations of the peptides have been found following chronic nicotine administration. Peptide levels, however, reflect the balance between biosynthesis and release of peptides in a tissue. Therefore, an altered activity of a peptidergic neuron might not be detectable, if a change in release is associated by a compensatory change in the biosynthesis of the peptide. The biosynthetic activity of a peptidergic neuron is reflected by the level of mRNA coding for the respective peptide precursor. Using RNA-hybridization techniques the effect of chronic nicotine treatment of rats on the tissue levels of mRNAs coding for the three opioid peptide precursors proopiomelanocortin (POMC), proenkephalin (PENK) and prodynorphin (PDYN)) is investigated in the chapter.