Clinical evidence has shown estrogen may delay the onset of Alzheimer's disease and protect against neuronal damage associated with stoke. Intracellular recordings (current-clamp) were made to characterize the effects of estrogen in the basolateral amygdala (BLA) of the rat brain. Excitatory postaynaptic potentials (EPSPs) were elicited by stimulation of afferents in the external capsule. Estrogen was found to decrease EPSPamplitude in a rapid (20-30 min) fashion. Similarly, reduction of spontaneous synaptic activity occurred upon estrogen treatment. EPSP amplitudes returned to normal within 20 minutes of estrogen washout. 4-hydroxy tamoxifen (4-OHT), and estrogen receptor antagonist, prevented the estrogen-induced decrease in EPSP amplitude, suggesting dependence on an estrogen receptor. Estrogen treatment had no effect on neuronal input resistance, accommodation response, resting membrane potential, or action potential firing frequency. Preliminary data showed no change in inhibitory postsynaptic potential (IPSP) amplitude, suggesting estrogen might act on the presynaptic cell. These findings imply that estrogen may be protecting neurons from excitotoxic injury associated with stroke through the modulation of glutamate release.