STRESS PERSISTENTLY INCREASES NMDA RECEPTOR-MEDIATED BINDING OF [H-3]PDBU (A MARKER FOR PROTEIN-KINASE-C) IN THE AMYGDALA, AND REEXPOSURE TO THE STRESSFUL CONTEXT REACTIVATES THE INCREASE

The long-term consequences of acute stress on [H-3]phorbol 12,13-dibut yrate ([H-3]PDBu) binding, a marker for protein kinase C (PKC) activit y, were investigated. In the first experiment, exposure to acute restr aint and intermittent tail-shock increased [H-3]PDBu binding in the am ygdala but not in the hippocampus or cerebral cortex. The increase was persistent, lasting at least 24 h after stressor cessation. In the se cond experiment, it was determined that the stress-induced increase in binding in the amygdala was dependent on NMDA receptor activation; ra ts injected with a competitive NMDA receptor antagonist prior to the s tressor did not exhibit the increased binding in the amygdala 24 h lat er. In the third experiment, re-exposure to the stressful context 96 h after stressor cessation reactivated the stress-induced increase the binding of [H-3]PDBu in the amygdala. Re-exposure to the context also increased binding in the thalamus and area CA1 of the hippocampus. [H- 3]PDBu binds preferentially to PKC in the membrane and, therefore, the se results suggest that stress induces the translocation of PKC from i ts resting compartments in the cytosol to the membrane. Its dependence on NMDA receptor activation implicates isoforms of PKC that are sensi tive to intracellular calcium, such as PKC gamma. The results further suggest that a 'psychological' manipulation, viz. context re-exposure, can reactivate the persistent increase in [H-3]PDBu binding in the am ygdala. (C) 1997 Elsevier Science B.V.