Format

Send to

Choose Destination
Toxicol Lett. 2018 Dec 13;302:35-41. doi: 10.1016/j.toxlet.2018.12.002. [Epub ahead of print]

Exposure to tobacco smoke during the early postnatal period modifies receptors and enzymes of the endocannabinoid system in the brainstem and striatum in mice.

Author information

1
Department of Clinical and Toxicological Analysis, School of Pharmaceutical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 580, bloco 13B, 05508-000, São Paulo, SP, Brazil; Department of Food and Drugs, School of Pharmaceutical Sciences, Federal University of Alfenas, Rua Gabriel Monteiro da Silva, 700, 37130-001, Alfenas, MG, Brazil.
2
Department of Clinical and Toxicological Analysis, School of Pharmaceutical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 580, bloco 13B, 05508-000, São Paulo, SP, Brazil.
3
Department of Biomedical Sciences and CNR Institute of Neuroscience, University of Cagliari, Cittadella Universitaria, Monserrato, CA, 09042, Italy.
4
Department of Clinical and Toxicological Analysis, School of Pharmaceutical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 580, bloco 13B, 05508-000, São Paulo, SP, Brazil. Electronic address: tmarcour@usp.br.

Abstract

Environmental tobacco smoke (ETS) exposure during brain development has been associated with several disorders, such as depression, anxiety, sudden infant death syndrome, and the predisposition to addiction. The endocannabinoid system plays an essential role in neuronal development. We investigated the effects of early postnatal ETS exposure on the endocannabinoid system in different brain regions. C57BL/6 J mice were exposed to ETS that was generated from 3R4F cigarettes from postnatal day 3 (P3) to P14. Receptors and enzymes of the endocannabinoid system were assessed in infancy, adolescence, and adulthood by Western blot. In the brainstem, ETS exposure decreased cannabinoid 1 (CB1) receptor, CB2 receptor, N-arachidonoyl phosphatidyl ethanol-specific phospholipase D (NAPE-PLD), and fatty acid amino hydrolase (FAAH) levels and increased in diacylglycerol lipase (DAGL) and monoacylglycerol lipase (MAGL) levels during infancy and decreased CB2 and FAAH levels during adulthood. In the striatum, ETS decreased in the NAPE-PLD and MAGL levels and increased FAAH levels during infancy, increased FAAH levels during adolescence, and decreased NAPE-PLD levels during adulthood. The present findings indicate that exposure to ETS during a critical period of brain development can disturb the endocannabinoid system in the brainstem and striatum, regions that are involved in the pathogenesis of sudden infant death syndrome and the susceptibility to addiction.

KEYWORDS:

Addiction; Brain; Cigarette smoke; Endocannabinoid system; Sudden infant death syndrome

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center