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Nicotinic Regulation of Adrenomedullary Opioid Peptide Synthesis and Secretion: A Model to Study Monoamine Neuropeptide Cotransmission

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Tobacco Smoking and Nicotine

Part of the book series: Advances in Behavioral Biology ((ABBI,volume 31))

Abstract

The adrenal medulla chromaffin cell synthesizes and stores in various subcellular compartments a number of proteins, peptides, nucleotides, and other small molecules to be secreted by Ca2+-dependent, nicotine receptor-mediated mechanism(s). Of these proteins and peptides, the enkephalins and other proenkephalin-derived opioid peptides are found in all species examined in substantial amounts, where they are costored with the catecholamines in the chromaffin vesicles. Splanchnic nerve stimulation, nicotine, and other secretagogues induce the cosecretion of these opioid peptides with the amines and other soluble components of these vesicles by the process of exocytosis. Regulatory mechanisms triggered by activation of nicotinic receptors, depolarization, and catecholamine depletion that involve cAMP-dependent and -independent mechanisms control the synthesis of enkephalins at the transcriptional, translational, and peptide processing levels. These mechanisms allow for rapid recovery of the opioid peptide content after secretion and for long-term modulation of the relative proportions and amounts in which catecholamines and enkephalins are costored and cosecreted. Opioid peptides secreted from the adrenal medulla reach ubiquitous opiate receptors throughout the organism and may modulate a number of important systemic functions including behavioral responses to stress. Enkephalins and norepinephrine also coexist in postganglionic sympathetic neurons, and some of the effects of nicotine administration may result from peripheral opiatergic responses through its powerful activation of the sympathetic system. The costorage and cosecretion of opioid peptides and catecholamines is only one of a growing number of examples of coexistence of multiple chemical messengers in single neurons or endocrine cells. This new principle of cotransmission is drastically changing our concepts and understanding of synaptic and endocrine function. Fast and slow dynamic changes in the ratios in which cotransmitters are stored and released and, thus, coact at the effector sites illustrate an unsuspected degree of synaptic plasticity. The exploration of the short-and long-term effects of chronic use of tobacco needs to take into consideration not only the effect of nicotine on classical transmitters but particularly how the biochemistry and function of these central and peripheral cotransmitter systems are being modified.

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© 1987 Plenum Press, New York

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Viveros, O.H., Unsworth, C.D., Kanamatsu, T., Hong, JS., Diliberto, E.J. (1987). Nicotinic Regulation of Adrenomedullary Opioid Peptide Synthesis and Secretion: A Model to Study Monoamine Neuropeptide Cotransmission. In: Martin, W.R., Van Loon, G.R., Iwamoto, E.T., Davis, L. (eds) Tobacco Smoking and Nicotine. Advances in Behavioral Biology, vol 31. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1911-5_22

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  • DOI: https://doi.org/10.1007/978-1-4613-1911-5_22

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4612-9063-6

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