Irwin J, Ahluwalia P, Anisman H
Brain Res. 1986 Jul 30;379(1):98-103. doi: 10.1016/0006-8993(86)90260-x.
Acute inescapable shock provokes an increase of norepinephrine (NE) utilization, leading to transient reductions of amine concentrations. In contrast, increased amine levels are evident after chronic shock, apparently because of a compensatory increase in synthesis. In acutely shocked animals subsequent re-exposure to even a limited amount of shock reinduced the NE reduction, whereas in chronically shocked mice a comparable re-exposure stressor increased amine levels and utilization. It is suggested that the mechanisms responsible for the amine release in acutely stressed animals, as well as those mechanisms subserving the increased amine levels evident after chronic stressor application, may be subject to conditioning or sensitization processes.
