ArticleBiological psychiatry2016
Overexpressing Corticotropin-Releasing Factor in the Primate Amygdala Increases Anxious Temperament and Alters Its Neural Circuit.
Article in Biological psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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49 citing papers in PubMed, 81 citations in OpenAlex.
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- Gene expression in the primate orbitofrontal cortex related to anxious temperament.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Efficient viral expression of a chemogenetic receptor in the old-world monkey amygdala.Current research in neurobiology · 2023Article
- Prefrontal influences on the function of the neural circuitry underlying anxious temperament in primates.Oxford open neuroscience · 2023Article
- DREADD-mediated amygdala activation is sufficient to induce anxiety-like responses in young nonhuman primates.Current research in neurobiology · 2023Article
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- Role of amygdala in stress-induced upregulation of airway IL-1 signaling in asthma.Biological psychology · 2022Article
- Evaluating depression- and anxiety-like behaviors in non-human primates.Frontiers in behavioral neuroscience · 2022Review
- Evidence in primates supporting the use of chemogenetics for the treatment of human refractory neuropsychiatric disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Infant inhibited temperament in primates predicts adult behavior, is heritable, and is associated with anxiety-relevant genetic variation.Molecular psychiatry · 2021Article
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16 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNonhuman primate models are critical for understanding mechanisms underlying human psychopathology. We established a nonhuman primate model of anxious temperament (AT) for studying the early-life risk to develop anxiety and depression. Studies have identified the central nucleus of the amygdala (Ce) as an essential component of AT's neural substrates. Corticotropin-releasing factor (CRF) is expressed in the Ce, has a role in stress, and is linked to psychopathology. Here, in young rhesus monkeys, we combined viral vector technology with assessments of anxiety and multimodal neuroimaging to understand the consequences of chronically increased CRF in the Ce region.
methodsUsing real-time intraoperative magnetic resonance imaging-guided convection-enhanced delivery, five monkeys received bilateral dorsal amygdala Ce-region infusions of adeno-associated virus serotype 2 containing the CRF construct. Their cagemates served as unoperated control subjects. AT, regional brain metabolism, resting functional magnetic resonance imaging, and diffusion tensor imaging were assessed before and 2 months after viral infusions.
resultsDorsal amygdala CRF overexpression significantly increased AT and metabolism within the dorsal amygdala. Additionally, we observed changes in metabolism in other AT-related regions, as well as in measures of functional and structural connectivity.
conclusionsThis study provides a translational roadmap that is important for understanding human psychopathology by combining molecular manipulations used in rodents with behavioral phenotyping and multimodal neuroimaging measures used in humans. The results indicate that chronic CRF overexpression in primates not only increases AT but also affects metabolism and connectivity within components of AT's neural circuitry.
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