CNS Developmental Issues (DOHAD Concept) Associated with Exposure to Pollutants during Gestation, Lactation/Infancy or Adolescence

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Environmental Neuroscience".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 476

Special Issue Editor


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Guest Editor
Laboratório de Neurofisiologia, Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro 20550-170, RJ, Brazil
Interests: nicotine; e-cigarette; adolescence

Special Issue Information

Dear Colleagues,

The impact of pollutants on human health has been systematically studied for more than a century now. The considerable amount of information amassed thus far notwithstanding, significant gaps in knowledge regarding the potential harmful effects of known pollutants, and of substances that may be considered as such, prevent the adoption of public policies that would result in stricter norms regarding safe environmental levels. Often, concentrations that are generally considered harmless for adults can result in severe insults to immature organisms, either by disrupting development in ways that immediately impact the individual’s health or by altering aspects of development that will result in late-onset, long-term health issues, in line with the Developmental Origins of Health and Diseases (DOHaD) concept. The brain is particularly vulnerable to insults during its ontogenetic development due to the complexity of the process as well as to the fact that it is one of the organs that takes longer to achieve its mature form. Thus, this Special Issues aims to address short- and long-term impacts that known and potential pollutants have on the development of brain structure and physiology as well as on metal health.

Dr. Alex Manhães
Guest Editor

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Keywords

  • nervous system
  • development
  • pollution
  • microplastics and nanoplastics
  • bisphenol
  • pesticides
  • PFAS/PFOS
  • petrochemicals

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Published Papers (1 paper)

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Research

22 pages, 1647 KiB  
Article
Nicotine’s Effects on Schizophrenia-like Symptoms in a Mice Model: Time Matters
by Ana Carolina Dutra-Tavares, Luciana Araújo Couto, Thainá P. Souza, Anais Bandeira-Martins, Juliana Oliveira Silva, Claudio C. Filgueiras, Anderson Ribeiro-Carvalho, Alex C. Manhães and Yael Abreu-Villaça
Brain Sci. 2024, 14(9), 855; https://doi.org/10.3390/brainsci14090855 - 25 Aug 2024
Viewed by 390
Abstract
Tobacco consumption in schizophrenia (SCHZ) patients is highly prevalent. Data support the occurrence of sequential events during comorbidity establishment, and both smoking first, SCHZ second and SCHZ first, smoking second sequences have been proposed. To investigate whether these two possibilities lead to distinct [...] Read more.
Tobacco consumption in schizophrenia (SCHZ) patients is highly prevalent. Data support the occurrence of sequential events during comorbidity establishment, and both smoking first, SCHZ second and SCHZ first, smoking second sequences have been proposed. To investigate whether these two possibilities lead to distinct outcomes of comorbidity, we used a phencyclidine-induced SCHZ model and nicotine exposure as a surrogate of smoking. C57Bl/6 mice were submitted to a protocol that either began with 4 days of phencyclidine exposure or 4 days of nicotine exposure. This period was followed by 5 days of combined phencyclidine + nicotine exposure. Locomotor sensitization and pre-pulse inhibition (PPI) were assessed due to their well-known associations with SCHZ as opposed to rearing, an unrelated behavior. Nicotine priming potentiated phencyclidine-evoked sensitization. However, nicotine exposure after SCHZ modeling did not interfere with phencyclidine’s effects. In the PPI test, nicotine after SCHZ modeling worsened the phencyclidine-evoked deficiency in males. In contrast, nicotine priming had no effects. Regarding rearing, nicotine priming failed to interfere with phencyclidine-mediated inhibition. Similarly, phencyclidine priming did not modify nicotine-mediated inhibition. The present results indicate that the sequence, either SCHZ-first or nicotine-first, differentially impacts comorbidity outcomes, a finding that is relevant for the identification of mechanisms of nicotine interference in the neurobiology of SCHZ. Full article
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