Serum corticosterone level predicts the magnitude of hippocampal primed burst potentiation and depression in urethane-anesthetized rats

Electrical stimulation of the hippocampal commissure with a pattern of pulses that mimics specific aspects of hippocampal physiological activity results in a long-lasting enhancement of the CA1 evoked response. We refer to this pattern-dependent increase in response as primed burst (PB) potentiation (Diamond, Dunwiddie, & Rose, 1988; Rose & Dunwiddie, 1986). The primary finding of the present study is that, in the urethane-anesthetized rat, there is a negative linear correlation between the magnitude of PB potentiation and elevated levels of serum corticosterone (r = −.76, p <.001). In contrast, there was no significant relationship between the magnitude of posttetanic potentiation (PTP) and the level of serum corticosterone (r =.13, p >.1). In addition, we observed a novel form of long-term depression of the population spike amplitude (PB depression) in recordings from 4 animals that had very high levels (> 60/μg/dl) of corticosterone. The magnitudes of PTP were not different across groups that developed PB potentiation (n = 9), no change in response (n = 7), or PB depression (n = 4). These findings suggest that corticosterone exerts a concentration-dependent inhibitory influence on long-term, but not short-term, hippocampal plasticity in the urethane-anesthetized rat. The present findings complement previous work indicating that stress-related adrenal hormones, and corticosterone in particular, can modulate behavioral learning and hippocampal plasticity.