Peter Salchner

TL;DR: The results suggest that the anxiogenic drugs selected activate a restricted set of forebrain areas that are consistent with the theory of an integrated forebrain and hindbrain neuronal system that is important for anxiety states evoked by both drug and environmental manipulations.

TL;DR: Deletion of the Y2 receptor may result in enhanced release of NPY, GABA and/or glutamate in brain areas linked to the manifestation of anxiety, and stress‐related behaviour such as the amygdala.

TL;DR: The present data indicate that the divergent anxiety-related behavioral response of HAB versus LAB rats to OF and OA exposures is associated with differential neuronal activation in restricted parts of the anxiety/fear circuitry.

TL;DR: Although the behavioral data confirmed the prediction that heightened trait anxiety would make rats more prone to experience stress, adrenocorticotropin and corticosterone were secreted to a higher extent in LABs than in HABs, in the latter, Fos expression upon SD was enhanced in the amygdala and hypothalamic areas compared with LABa.

TL;DR: The detection of similarly disturbed activation patterns in a key set of anxiety-related brain areas in two independent models reflecting psychopathological states of trait anxiety confirms the notion that the altered brain activation in HAB animals is indeed characteristic of enhanced (pathological) anxiety, providing information for potential targets of therapeutic intervention.