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Almost by definition, learning and the effect of stress on learning represent modifications of existing neuronal circuitry. Under some circumstances, this modification can be measured electrophysiologically. One such measure of plasticity is long-term potentiation (LTP), a long-lasting increase in synaptic efficacy following brief exposure to tetanic stimulation. In 1987, Foy et al. reported that hippocampal LTP was impaired by exposure to inescapable shock. We have recent evidence that the impairment in LTP can be prevented by allowing the animal to learn to escape the shock (Shors et al., 1989), indicating that the stress effect is to some extent mediated by "psychological" variables. Regardless of LTP's putative role in learning and memory processes, such a stress-induced decrease in neuronal plasticity is likely to have profound effects on the behaving organism.

Electrophysiological field potentials recorded from in vitro hippocampal slice preparations show dose-dependent differences in response to 17-beta-estradiol (E2) and delta-9-tetrahydrocannabinol (THC) added to the incubation medium. Using a wide range of doses (1 pM-10 nM), it was found that mid-range concentrations of estradiol (100 pM) and THC (10 pM) tended to increase field potentials in CA1 of rodents. Higher dose levels of each agent were found to depress neuronal activity. In the context of prior findings, these results suggest that the two compounds share a common mechanism of action in the hippocampus.

Electrophysiological field potentials recorded from in vitro hippocampal slice preparations show responses to exogenous gonadal steroids added to the incubation medium. The peak effect of the addition of 17-beta-estradiol occurred at a 100 pmol concentration; the CA1 field potential was increased by an average of 148 percent. 17-alpha-estradiol, often used as a negative control in experiments demonstrating estrogen specificity of receptor binding sites and biological responses, had no effect on field potentials following addition of drug to the incubation medium. The addition of a 100 pmol concentration of 17-beta-estradiol to the same slices which had been pretreated with 17-alpha-estradiol, blocked the facilitatory response elicited by the 17-beta-estradiol administered alone. Since no enhancement of the field potential is observed with 17-beta-estradiol following pretreatment of 17-alpha-estradiol, this would support the hypothesis that hippocampal modulation by gonadal steroid hormones may be due to involvement of an estrogen receptor mediated phenomena.