Neuropsychiatric disorders including mood disorders, autism spectrum disorders, and schizophrenia typically have multiple genetic and environmental factors interacting to result in significant changes in gene expression patterns across the developmental period that modify brain physiology and neural circuit function. This includes cell-type specific changes that contribute to pathology. Understanding the gene expression changes contributing to maladaptive circuit function or cellular physiology is difficult to perform on tissues from human subjects due to lack of availability of post-mortem samples, differences in postmortem interval, or the absence of environmental factors that are naturally occurring (maternal factors and peripheral circuits) in the development of stem-cell derived brain organoids. Animal models of neuropsychiatric disorder offer etiologically valid systems to further explore disease development, underlying mechanisms, and treatments. These discoveries are enhanced by transcriptomic approaches including gene expression profiling of brain areas and cell-type specific transcriptomic approaches such as ribosome affinity purification, or single cell sequencing.
Our goal is to feature transcriptomic studies, including gene expression profiling of brain areas, cell-type specific transcriptomic approaches such as ribosome affinity purification or single cell sequencing, and integrative multiomics studies, in animal models of neuropsychiatric disorders. We aim to underscore how they can be used for basic research of pathway discovery, gene discovery, mechanistic understanding of the disease, and adaptation to environmental risk factors. We also seek to highlight how transcriptomic and gene expression studies can be utilized in applied research for understanding the mechanisms of current therapeutic treatments as well as development of future therapeutic treatments.
Neuropsychiatric disorders considered include, but are not limited to, autism spectrum disorders, syndromes associated with intellectual disability, attention-deficit hyperactivity disorder, tic disorders, mood disorders, obsessive-compulsive disorder, and schizophrenia.
• Animal models of neuropsychiatric disease including transgenic models, optogenetic manipulation of circuits, biochemical or environmental manipulation, or spontaneously occurring models such as self-injurious behaviors in primates or spontaneously hypertensive rats.
• Bulk-RNA sequencing studies, single cell sequencing studies or other large-scale transcriptomic approaches that employ the models listed above.
• RT-PCR and molecular studies that focus on specific disorders, cell types, or pathways involved in neuropsychiatric disorders.
• Transcriptomic studies using animal models that focus on risk factors for neuropsychiatric disorders including stress (e.g., chronic unpredictable stress, early life stress, social defeat stress), or prenatal exposures.
Keywords:
RNASeq, depression, gene expression, mouse, rhesus macaque
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Neuropsychiatric disorders including mood disorders, autism spectrum disorders, and schizophrenia typically have multiple genetic and environmental factors interacting to result in significant changes in gene expression patterns across the developmental period that modify brain physiology and neural circuit function. This includes cell-type specific changes that contribute to pathology. Understanding the gene expression changes contributing to maladaptive circuit function or cellular physiology is difficult to perform on tissues from human subjects due to lack of availability of post-mortem samples, differences in postmortem interval, or the absence of environmental factors that are naturally occurring (maternal factors and peripheral circuits) in the development of stem-cell derived brain organoids. Animal models of neuropsychiatric disorder offer etiologically valid systems to further explore disease development, underlying mechanisms, and treatments. These discoveries are enhanced by transcriptomic approaches including gene expression profiling of brain areas and cell-type specific transcriptomic approaches such as ribosome affinity purification, or single cell sequencing.
Our goal is to feature transcriptomic studies, including gene expression profiling of brain areas, cell-type specific transcriptomic approaches such as ribosome affinity purification or single cell sequencing, and integrative multiomics studies, in animal models of neuropsychiatric disorders. We aim to underscore how they can be used for basic research of pathway discovery, gene discovery, mechanistic understanding of the disease, and adaptation to environmental risk factors. We also seek to highlight how transcriptomic and gene expression studies can be utilized in applied research for understanding the mechanisms of current therapeutic treatments as well as development of future therapeutic treatments.
Neuropsychiatric disorders considered include, but are not limited to, autism spectrum disorders, syndromes associated with intellectual disability, attention-deficit hyperactivity disorder, tic disorders, mood disorders, obsessive-compulsive disorder, and schizophrenia.
• Animal models of neuropsychiatric disease including transgenic models, optogenetic manipulation of circuits, biochemical or environmental manipulation, or spontaneously occurring models such as self-injurious behaviors in primates or spontaneously hypertensive rats.
• Bulk-RNA sequencing studies, single cell sequencing studies or other large-scale transcriptomic approaches that employ the models listed above.
• RT-PCR and molecular studies that focus on specific disorders, cell types, or pathways involved in neuropsychiatric disorders.
• Transcriptomic studies using animal models that focus on risk factors for neuropsychiatric disorders including stress (e.g., chronic unpredictable stress, early life stress, social defeat stress), or prenatal exposures.
Keywords:
RNASeq, depression, gene expression, mouse, rhesus macaque
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.