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Cher V. Masini

Researcher at University of Colorado Boulder

Publications -  25
Citations -  1356

Cher V. Masini is an academic researcher from University of Colorado Boulder. The author has contributed to research in topics: Habituation & Corticosterone. The author has an hindex of 18, co-authored 25 publications receiving 1247 citations.

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The pattern of brain c-fos mRNA induced by a component of fox odor, 2,5-dihydro-2,4,5-trimethylthiazoline (TMT), in rats, suggests both systemic and processive stress characteristics.

TL;DR: The results suggest that TMT elicits stress responses through a relatively unique and complex mix of brain regions associated with both processive and systemic neural pathways, unlike those seen in response to cat odors.
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Controllable versus uncontrollable stressors bi-directionally modulate conditioned but not innate fear

TL;DR: The impact of exposure to a stressor in a different environment on subsequent fear conditioning and extinction, and whether the degree of behavioral control that the subject has over the stressor is of importance is examined.
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Ferret Odor as a Processive Stress Model in Rats: Neurochemical, Behavioral, and Endocrine Evidence

TL;DR: It is suggested that ferret odor produces a reliable unconditioned stress response and may be useful as a processive stress model.
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Sex differences in activated corticotropin-releasing factor neurons within stress-related neurocircuitry and hypothalamic-pituitary-adrenocortical axis hormones following restraint in rats.

TL;DR: Data suggest sex differences in HPA axis activation in response to perceived threat may be influenced by specific populations of CRF neurons in key stress-related brain regions, the BSTav, MPOA, and PVN, which may be independent of circulating sex steroids.
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Hypothalamic Pituitary Adrenal Axis Responses to Low‐Intensity Stressors are Reduced After Voluntary Wheel Running in Rats

TL;DR: Evidence is provided that in rats, 6 weeks of daily or intermittent exercise constrains the HPA axis response to mild, but not more intense stressors, and that this regulation may be mediated at a central level beyond the primary sensory input.