Stress persistently increases NMDA receptor-mediated binding of [H]PDBu (a marker for protein kinase C) in the amygdala, and re-exposure to the stressful context reactivates the increase

The long-term consequences of acute stress on ³H]phorbol 12,13-dibutyrate (³H]PDBu) binding, a marker for protein kinase C (PKC) activity, were investigated. In the first experiment, exposure to acute restraint and intermittent tail-shock increased ³H]PDBu binding in the amygdala but not in the hippocampus or cerebral cortex. The increase was persistent, lasting at least 24 h after stressor cessation. In the second experiment, it was determined that the stress-induced increase in binding in the amygdala was dependent on NMDA receptor activation; rats injected with a competitive NMDA receptor antagonist prior to the stressor did not exhibit the increased binding in the amygdala 24 h later. In the third experiment, re-exposure to the stressful context 96 h after stressor cessation reactivated the stress-induced increase the binding of ³H]PDBu in the amygdala. Re-exposure to the context also increased binding in the thalamus and area CA1 of the hippocampus. ³H]PDBu binds preferentially to PKC in the membrane and, therefore, these results suggest that stress induces the translocation of PKC from its resting compartments in the cytosol to the membrane. Its dependence on NMDA receptor activation implicates isoforms of PKC that are sensitive to intracellular calcium, such as PKCγ. The results further suggest that a ‘psychological' manipulation, viz. context re-exposure, can reactivate the persistent increase in ³H]PDBu binding in the amygdala. © 1997 Elsevier Science B.V. All rights reserved.