Modulation of CaV1.2 Channel Function by Interacting Proteins and Post-Translational Modifications: Implications in Cardiovascular Diseases and COVID-19

Handbook of experimental pharmacology, Journal Year: 2023, Volume and Issue: unknown, P. 83 - 103

Published: Jan. 1, 2023

Language: Английский

The effects of paroxetine-induced transient apoptosis and brain remodeling on social behavior in developing zebrafish

Research Square (Research Square), Journal Year: 2023, Volume and Issue: unknown

Published: Nov. 14, 2023

Abstract Autism spectrum disorder (ASD) is a neurodevelopmental condition caused by various genetic and environmental factors. This has the cardinal symptoms including impaired social behavior involving amygdala. Antidepressants such as paroxetine in early pregnancy increase risk of ASD offspring. However, comprehensive picture underlying pathogenic mechanisms remains elusive. Here, we demonstrate that exposure zebrafish embryos to suppresses neurogenesis optic tectum dorsal telencephalon which corresponds human Paroxetine-treated exhibit growth, with small heads short body lengths resulting from transient apoptosis. reminiscent early-onset fetal growth restriction (FGR) associated ASD. Interestingly, suppressed was found be restored after cessation paroxetine. accompanied extended retinotectal projections, suggesting brain-preferential remodeling. Finally, paroxetine-treated fish exhibited behavior, further supporting correspondence Our findings offer new insights into etiology

Language: Английский

The effects of paroxetine-induced transient apoptosis and brain remodeling on social behavior in developing zebrafish

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2023, Volume and Issue: unknown

Published: Nov. 13, 2023

Abstract Autism spectrum disorder (ASD) is a neurodevelopmental condition caused by various genetic and environmental factors. This has the cardinal symptoms including impaired social behavior involving amygdala. Antidepressants such as paroxetine in early pregnancy increase risk of ASD offspring. However, comprehensive picture underlying pathogenic mechanisms remains elusive. Here, we demonstrate that exposure zebrafish embryos to suppresses neurogenesis optic tectum dorsal telencephalon which corresponds human Paroxetine-treated exhibit growth, with small heads short body lengths resulting from transient apoptosis. reminiscent early-onset fetal growth restriction (FGR) associated ASD. Interestingly, suppressed was found be restored after cessation paroxetine. accompanied extended retinotectal projections, suggesting brain-preferential remodeling. Finally, paroxetine-treated fish exhibited behavior, further supporting correspondence Our findings offer new insights into etiology

Language: Английский