Publications by authors named "Trevonn Gyles"
Background: Early life stress (ELS) refers to exposure to negative childhood experiences, such as neglect, disaster, and physical, mental, or emotional abuse. ELS can permanently alter the brain, leading to cognitive impairment, increased sensitivity to future stressors, and mental health risks. The prefrontal cortex (PFC) is a key brain region implicated in the effects of ELS.
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- Astrocytes in the nucleus accumbens (NAc) have been shown to play a significant role in stress and depression, but their transcriptional responses to stress were not well understood prior to this study.
- Using methods like RNA-sequencing and immunohistochemistry, researchers investigated how chronic social defeat stress (CSDS) affects the transcriptome of NAc astrocytes in male mice.
- The findings revealed a strong transcriptional response in astrocytes linked to CREB activation, which influences whether a mouse becomes stress-resilient or stress-susceptible, highlighting the potential of astrocytes in understanding neuropsychiatric disorders.
Article Synopsis
- Major depressive disorder (MDD) is associated with changes in brain structure and synaptic function, particularly in limbic regions.
- Astrocytes, brain cells affected by chronic stress, show altered gene profiles that may play a role in these changes, especially in the nucleus accumbens (NAc).
- The study found that a specific astrocyte-produced protease gene is downregulated in males and upregulated in females, revealing sex-specific responses to stress and offering potential new targets for MDD treatment.
Background: Increasing evidence implicates astrocytes in stress and depression in both rodent models and human Major Depressive Disorder (MDD). Despite this, little is known about the transcriptional responses to stress of astrocytes within the nucleus accumbens (NAc), a key brain reward region, and their influence on behavioral outcomes.
Methods: We used whole cell sorting, RNA-sequencing, and bioinformatic analyses to investigate the NAc astrocyte transcriptome in male mice in response to chronic social defeat stress (CSDS).
Advancing preclinical chronic stress models to promote therapeutic discovery for human stress disorders.
Neuropsychopharmacology
January 2024
There is an urgent need to develop more effective treatments for stress-related illnesses, which include depression, post-traumatic stress disorder, and anxiety. We view animal models as playing an essential role in this effort, but to date, such approaches have generally not succeeded in developing therapeutics with new mechanisms of action. This is partly due to the complexity of the brain and its disorders, but also to inherent difficulties in modeling human disorders in rodents and to the incorrect use of animal models: namely, trying to recapitulate a human syndrome in a rodent which is likely not possible as opposed to using animals to understand underlying mechanisms and evaluating potential therapeutic paths.
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- Newborns acquire maternal microbiota during birth, which is crucial for their health and development, but the individual differences in these microbial communities and their impacts on health are not fully understood.
- Researchers created a model using fetal mice that mimics the microbial exposure of vaginal birth, showing significant effects on metabolism, immunity, and brain development in offspring based on the specific communities introduced.
- The study found that an unhealthy prenatal environment (like maternal obesity or dysbiosis) can worsen health outcomes and increase mortality in offspring, highlighting the importance of the maternal microbiome and prenatal conditions on later health.
Background: Major depressive disorder is prevalent in children and adolescents and is associated with a high degree of morbidity throughout life, with potentially devastating personal consequences and public health impact. The efficacy of ketamine (KET) as an antidepressant has been demonstrated in adolescent rodents; however, the neurobiological mechanisms underlying these effects are unknown. Recent evidence showed that KET reverses stress-induced (i.
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