New Insights and New Issues in Developmental Neurotoxicology
Section snippets
INTRODUCTION
A wide variety of neuropsychiatric disturbances, ranging from mental retardation to schizophrenia, are believed to be the result of a combination of genetic and environmental influences, the latter impinging on the immature brain during critical stages of development. We have been exploring mechanisms by which environmental factors can disrupt development of the brain, thereby giving rise to neurobehavioral disturbances that may be expressed either in childhood or with delayed onset in
CONCLUDING REMARKS
Here, I have summarized recent findings pertaining to several environmental agents (ethanol, PCP, ketamine, nitrous oxide, barbiturates, benzodiazepines, halothane, isoflurane, propofol, phenytoin, valproate) that have the potential to delete large numbers of neurons from the developing brain by a newly discovered mechanism involving interference in the action of neurotransmitters (Glu and GABA) at NMDA and GABAA receptors during the synaptogenesis period, also known as the brain growth spurt
Acknowledgements
Supported by NIH Grants AG 11355, DA 05072, HD 37100, EY 08089, and a NARSAD Toulmin Distinguished Investigator Award.
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2018, Schizophrenia ResearchCitation Excerpt :In our study, this domain has also turned out to be a significant predictor of recovery among patients with a FEP. Overall, the cause of cognitive deficits in psychotic disorders is still not clear; several etiological hypotheses have been postulated, such as the glutamate hypothesis, where cognitive disorders can be a consequence of the neurotoxic activity (Olney, 2002; Stahl, 2004). Other views involve reduced brain-derived neurotrophic factor (BDNF) levels (Buckley et al., 2007; Durany et al., 2001; Ikeda et al., 2008) which has been linked to cognitive performance (Aas et al., 2013).