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Orellana JA, Busso D, Ramírez G, et al. Prenatal nicotine exposure enhances Cx43 and Panx1 unopposed channel activity in brain cells of adult offspring mice fed a high-fat/cholesterol diet. Front Cell Neurosci. 2014;8:403doi: 10.3389/fncel.2014.00403.
Orellana, J. A., Busso, D., Ramírez, G., Campos, M., Rigotti, A., Eugenín, J., & von Bernhardi, R. (2014). Prenatal nicotine exposure enhances Cx43 and Panx1 unopposed channel activity in brain cells of adult offspring mice fed a high-fat/cholesterol diet. Frontiers in cellular neuroscience, 8403. https://doi.org/10.3389/fncel.2014.00403
Orellana, Juan A, et al. "Prenatal nicotine exposure enhances Cx43 and Panx1 unopposed channel activity in brain cells of adult offspring mice fed a high-fat/cholesterol diet." Frontiers in cellular neuroscience vol. 8 (2014): 403. doi: https://doi.org/10.3389/fncel.2014.00403
Orellana JA, Busso D, Ramírez G, Campos M, Rigotti A, Eugenín J, von Bernhardi R. Prenatal nicotine exposure enhances Cx43 and Panx1 unopposed channel activity in brain cells of adult offspring mice fed a high-fat/cholesterol diet. Front Cell Neurosci. 2014 Dec 02;8:403. doi: 10.3389/fncel.2014.00403. eCollection 2014. PMID: 25520621; PMCID: PMC4251442.
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Front Cell Neurosci. 2014 Dec 02;8:403. doi: 10.3389/fncel.2014.00403. eCollection 2014.

Prenatal nicotine exposure enhances Cx43 and Panx1 unopposed channel activity in brain cells of adult offspring mice fed a high-fat/cholesterol diet.

Frontiers in cellular neuroscience

Juan A Orellana, Dolores Busso, Gigliola Ramírez, Marlys Campos, Attilio Rigotti, Jaime Eugenín, Rommy von Bernhardi

Affiliations

  1. Departamento de Neurología, Escuela de Medicina, Pontificia Universidad Católica de Chile Santiago, Chile.
  2. Departamento de Nutrición, Diabetes y Metabolismo, Escuela de Medicina, Pontificia Universidad Católica de Chile Santiago, Chile ; Centro de Nutrición Molecular y Enfermedades Crónicas, Escuela de Medicina, Pontificia Universidad Católica de Chile Santiago, Chile.
  3. Laboratorio de Sistemas Neurales, Departamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile Santiago, Chile.

PMID: 25520621 PMCID: PMC4251442 DOI: 10.3389/fncel.2014.00403

Abstract

Nicotine, the most important neuroteratogen of tobacco smoke, can reproduce brain and cognitive disturbances per se when administered prenatally. However, it is still unknown if paracrine signaling among brain cells participates in prenatal nicotine-induced brain impairment of adult offspring. Paracrine signaling is partly mediated by unopposed channels formed by connexins hemichannels (HCs) and pannexins serving as aqueous pores permeable to ions and small signaling molecules, allowing exchange between the intra- and extracellular milieus. Our aim was to address whether prenatal nicotine exposure changes the activity of those channels in adult mice offspring under control conditions or subjected to a second challenge during young ages: high-fat/cholesterol (HFC) diet. To induce prenatal exposure to nicotine, osmotic minipumps were implanted in CF1 pregnant mice at gestational day 5 to deliver nicotine bitartrate or saline (control) solutions. After weaning, offspring of nicotine-treated or untreated pregnant mice were fed ad libitum with chow or HFC diets for 8 weeks. The functional state of connexin 43 (Cx43) and pannexin 1 (Panx1) unopposed channels was evaluated by dye uptake experiments in hippocampal slices from 11-week-old mice. We found that prenatal nicotine increased the opening of Cx43 HCs in astrocytes, and Panx1 channels in microglia and neurons only if offspring mice were fed with HFC diet. Blockade of inducible nitric oxide synthase (iNOS), cyclooxygenase 2 (COX2) and prostaglandin E receptor 1 (EP1), ionotropic ATP receptor type 7 (P2X7) and NMDA receptors, showed differential inhibition of prenatal nicotine-induced channel opening in glial cells and neurons. Importantly, inhibition of the above mentioned enzymes and receptors, or blockade of Cx43 and Panx1 unopposed channels greatly reduced adenosine triphosphate (ATP) and glutamate release from hippocampal slices of prenatally nicotine-exposed offspring. We propose that unregulated gliotransmitter release through Cx43 and Panx1 unopposed channels may participate in brain alterations observed in offspring of mothers exposed to tobacco smoke during pregnancy.

Keywords: brain; connexins; fat diet; glia; hemichannels; nicotine; pannexins

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