Esther L. Sabban

TL;DR: Data summarized here indicate that catecholaminergic systems are activated in different ways following exposure to distinct stressful stimuli.

TL;DR: These studies suggest that dynamic interplay is involved in converting the transient increases in the rate of transcription into prolonged (potentially adaptive or maladaptive) changes in gene expression.

TL;DR: The results suggest that endogenous glucocorticoids restrain responses of catecholamine turnover, synthesis, release, reuptake, and metabolism during stress, and suggest that a nonneuronal, nonpituitary factor contributes to TH gene expression during some forms of stress, whereas pituitary-adrenocortical factors play the essential role in the regulation of PNMT gene expression.

TL;DR: It is raised the possibility that regulation of tyrosine hydroxylase in the LC represents an adaptive response of LC neurons to antidepressants that mediates some of their therapeutic actions in depression and/or other psychiatric disturbances.

TL;DR: Results show that single IN NPY can alter stress-triggered dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and activation of central noradrenergic activity.