Transient and persistent consequences of acute stress on long-term potentiation (LTP), synaptic efficacy, theta rhythms and bursts in area CA1 of the hippocampus.

Previous studies reported that exposure to an acute stressor of restraint and intermittent tailshock impairs long-term potentiation (LTP) in area CA1 of the rat hippocampus. In the first experiment, the longevity of the stress-induced impairment of LTP was determined. LTP of the excitatory postsynaptic potential (EPSP) was impaired 2 but not 4 days after stressor cessation. Exposure to the stressor also persistently enhanced the synaptic response to the tetanic stimulation patterned after theta rhythm activity (10, 100 Hz bursts delivered at 5 Hz). In a second experiment, we tested the hypothesis that exposure to the stressor enhanced synaptic efficacy itself. EPSPs were recorded from freely moving rats before, during and after stressor exposure. The synaptic response was not enhanced during stressor exposure. Instead, cessation of the stressor (and perhaps movement associated with release from restraint) induced a transient (< 2 min) decrease in synaptic efficacy. To determine whether exposure to the stressor enhances endogenous theta rhythms in area CA1, electroencephalographic (EEG) recordings were obtained from freely moving rats before, during and after exposure to the stressor. The power of theta (4-8 Hz) and low frequency (0.1-3.9 Hz) activity was enhanced in response to the tailshock aspect of the stressor. Together, the results indicate that exposure to an acute stressful event increases theta activity and its cessation transiently decreases synaptic efficacy. These transient effects are succeeded by a persistently sensitized response to theta burst stimulation and impaired LTP.