Exposure to nicotine and withdrawal in Wistar rats: an electrophysiological study.

Nicotine cardiac electrophysiology electroencephalography substance-related disorder withdrawal

Journal

Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco
ISSN: 1469-994X
Titre abrégé: Nicotine Tob Res
Pays: England
ID NLM: 9815751

Informations de publication

Date de publication:
12 Oct 2024
Historique:
received: 26 02 2024
medline: 12 10 2024
pubmed: 12 10 2024
entrez: 12 10 2024
Statut: aheadofprint

Résumé

Throughout the world, smoking is one of the principal causes of preventable death. Nicotine, the primary active component of tabacco, acts as a psychostimulant and modulates the electrical activity of a number of the areas of the brain involved in addiction. Abstinence from nicotine will also impact the functional state of the brain, which is reflected in symptoms of craving and susceptibility to relapse. In addition, given the increase in the sympathetic tone of the heart and pulse rate promoted by nicotine, its consumption can contribute to tachyarrhythmia. The present study investigated the electroencephalographic (EEG) and electrocardiographic (ECG) patterns of Wistar rats submitted to acute or chronic exposure to nicotine, followed by withdrawal for 24 or 48 hours, and the re-administration (or not) of nicotine, to simulate episodes of relapse. The EEG data revealed an increase in all types of brainwaves, with emphasis on high-frequency (alpha, beta, and gamma) brain oscillations following both acute and chronic exposure to nicotine (14 days), whereas in withdrawal, there was a predominancy of delta waves. When exposure to nicotine was reinstated after withdrawal, the observed EEG profile was similar to that found in chronic exposure. The electrocardiogram reads showed that both acute and chronic exposure to nicotine caused abnormalities in the atrioventricular conduction and that, while these changes improve with substance withdrawal, relapse can worsen these parameters. The results of this study indicate that high-frequency brainwaves are correlated with nicotine dependence, while slow brain oscillations are consistent with drug craving, and episodes of nicotine relapse can reproduce brain activity patterns linked to dependence. Finally, exposure to nicotine predisposes the individual to heart rhythm abnormalities, which are attenuated by withdrawal, but may nevertheless be restored rapidly with re-exposure to the substance. This study demonstrated that nicotine increases high-frequency brain oscillations, which is associated with addiction, whereas withdrawal elevates the delta wave power, suggesting craving. Re-exposure to nicotine following withdrawal restores rapidly the EEG profile of chronic dependence. In addition, nicotine has deleterious impacts on cardiac activity, which are linked to fatal arrhythmias. This implies that stopping smoking is beneficial for the amelioration of the alterations in heart rhythm caused by nicotine addiction. This study elucidates the functional states of the brain and heart during both sporadic and chronic nicotine use, and the electrophysiological explanation for substance dependence and drug relapse after craving episodes.

Identifiants

pubmed: 39394893
pii: 7819318
doi: 10.1093/ntr/ntae240
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© The Author(s) 2024. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.

Auteurs

Allan Carlos da Silva Tiago (AC)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Suzane Maia da Fonseca (SM)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Esther Padilha da Silveira (E)

Laboratory of Experimental Neuropathology. Institute of Biological Sciences, Federal University of Pará.

Vitoria Corrêa Santos (VC)

Laboratory of Experimental Neuropathology. Institute of Biological Sciences, Federal University of Pará.

Fernanda Myllena Sousa Campos (FMS)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Danielma Carvalho de Lima (D)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Mariana Kondo Obara (MK)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Rafaella Marques Ribeiro (RM)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

João Cleiton Martins Rodrigues (JCM)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Marcos Vinícius Cardoso Reis (MVC)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Maria Klara Otake Hamoy (MKO)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Josuelem Portela Castro (JP)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Walace Gomes Leal (W)

Laboratory of Experimental Neuroprotection and Neurodegeneration. Morphophysiology Unit. Tapajós Campus. Federal University of Western Pará.

Dielly Catrina Favacho Lopes (DC)

Laboratory of Experimental Neuropathology. Institute of Biological Sciences, Federal University of Pará.

Moisés Hamoy (M)

Laboratory of the Pharmacology and Toxicology of Natural Products, Institute of Biological Sciences, Federal University of Pará.

Classifications MeSH