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Endogenous Cholinergic Neurotransmission Contributes to Behavioral Sensitization to Morphine

Neuroplasticity in the mesolimbic dopaminergic system is critical for behavioral adaptations associated with opioid reward and addiction. These processes may be influenced by cholinergic transmission arising from the laterodorsal tegmental nucleus (LDTg), a main source of acetylcholine to mesolimbic...

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Autores principales: Bajic, Dusica, Soiza-Reilly, Mariano, Spalding, Allegra L., Berde, Charles B., Commons, Kathryn G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315441/
https://www.ncbi.nlm.nih.gov/pubmed/25647082
http://dx.doi.org/10.1371/journal.pone.0117601
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author Bajic, Dusica
Soiza-Reilly, Mariano
Spalding, Allegra L.
Berde, Charles B.
Commons, Kathryn G.
author_facet Bajic, Dusica
Soiza-Reilly, Mariano
Spalding, Allegra L.
Berde, Charles B.
Commons, Kathryn G.
author_sort Bajic, Dusica
collection PubMed
description Neuroplasticity in the mesolimbic dopaminergic system is critical for behavioral adaptations associated with opioid reward and addiction. These processes may be influenced by cholinergic transmission arising from the laterodorsal tegmental nucleus (LDTg), a main source of acetylcholine to mesolimbic dopaminergic neurons. To examine this possibility we asked if chronic systemic morphine administration affects expression of genes in ventral and ventrolateral periaqueductal gray at the level of the LDTg using rtPCR. Specifically, we examined gene expression changes in the area of interest using Neurotransmitters and Receptors PCR array between chronic morphine and saline control groups. Analysis suggested that chronic morphine administration led to changes in expression of genes associated, in part, with cholinergic neurotransmission. Furthermore, using a quantitative immunofluorescent technique, we found that chronic morphine treatment produced a significant increase in immunolabeling of the cholinergic marker (vesicular acetylcholine transporter) in neurons of the LDTg. Finally, systemic administration of the nonselective and noncompetitive neuronal nicotinic antagonist mecamylamine (0.5 or 2 mg/kg) dose-dependently blocked the expression, and to a lesser extent the development, of locomotor sensitization. The same treatment had no effect on acute morphine antinociception, antinociceptive tolerance or dependence to chronic morphine. Taken together, the results suggest that endogenous nicotinic cholinergic neurotransmission selectively contributes to behavioral sensitization to morphine and this process may, in part, involve cholinergic neurons within the LDTg.
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spelling pubmed-43154412015-02-13 Endogenous Cholinergic Neurotransmission Contributes to Behavioral Sensitization to Morphine Bajic, Dusica Soiza-Reilly, Mariano Spalding, Allegra L. Berde, Charles B. Commons, Kathryn G. PLoS One Research Article Neuroplasticity in the mesolimbic dopaminergic system is critical for behavioral adaptations associated with opioid reward and addiction. These processes may be influenced by cholinergic transmission arising from the laterodorsal tegmental nucleus (LDTg), a main source of acetylcholine to mesolimbic dopaminergic neurons. To examine this possibility we asked if chronic systemic morphine administration affects expression of genes in ventral and ventrolateral periaqueductal gray at the level of the LDTg using rtPCR. Specifically, we examined gene expression changes in the area of interest using Neurotransmitters and Receptors PCR array between chronic morphine and saline control groups. Analysis suggested that chronic morphine administration led to changes in expression of genes associated, in part, with cholinergic neurotransmission. Furthermore, using a quantitative immunofluorescent technique, we found that chronic morphine treatment produced a significant increase in immunolabeling of the cholinergic marker (vesicular acetylcholine transporter) in neurons of the LDTg. Finally, systemic administration of the nonselective and noncompetitive neuronal nicotinic antagonist mecamylamine (0.5 or 2 mg/kg) dose-dependently blocked the expression, and to a lesser extent the development, of locomotor sensitization. The same treatment had no effect on acute morphine antinociception, antinociceptive tolerance or dependence to chronic morphine. Taken together, the results suggest that endogenous nicotinic cholinergic neurotransmission selectively contributes to behavioral sensitization to morphine and this process may, in part, involve cholinergic neurons within the LDTg. Public Library of Science 2015-02-03 /pmc/articles/PMC4315441/ /pubmed/25647082 http://dx.doi.org/10.1371/journal.pone.0117601 Text en © 2015 Bajic et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Bajic, Dusica
Soiza-Reilly, Mariano
Spalding, Allegra L.
Berde, Charles B.
Commons, Kathryn G.
Endogenous Cholinergic Neurotransmission Contributes to Behavioral Sensitization to Morphine
title Endogenous Cholinergic Neurotransmission Contributes to Behavioral Sensitization to Morphine
title_full Endogenous Cholinergic Neurotransmission Contributes to Behavioral Sensitization to Morphine
title_fullStr Endogenous Cholinergic Neurotransmission Contributes to Behavioral Sensitization to Morphine
title_full_unstemmed Endogenous Cholinergic Neurotransmission Contributes to Behavioral Sensitization to Morphine
title_short Endogenous Cholinergic Neurotransmission Contributes to Behavioral Sensitization to Morphine
title_sort endogenous cholinergic neurotransmission contributes to behavioral sensitization to morphine
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315441/
https://www.ncbi.nlm.nih.gov/pubmed/25647082
http://dx.doi.org/10.1371/journal.pone.0117601
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