Electrical stimulation of the medial amygdala (AMY) elicited antidromicaction potentials in neurons in the preoptic area (POA) and the lateralseptum (LS) of 36 urethane-anesthetized ovariectomized female rats, whichwere either treated with estrogen o not treated. The extracellular potentialsfrom the two sites showed similar characteristics, with the exception of thesensitivity to estrogen: they had latencies between 3 and 35 ms. Thresholdswere as low as 100 microA. The mean relative refractory period was 2.2 ms.The peak-to-peak amplitudes of the positive-negative biphasic potentialranged from 1.0 mV to 12.0 mV. Estrogen had site-specific effects onparameters of antidromic activation in the POA. Estrogen-treated rats had asignificantly higher threshold (937 vs 664 microA) and a longer refractoryperiod (2.5 vs 2.1 ms) than the ovariectomized rats (P < 0.05 for each). Theeffects were absent in the LS. Selective cutting of the stria terminalisdiminished the AMY-induced antidromic responses in the POA and LS. Electricalstimulation of the stria blocked the AMY-induced antidromic potentials bycollision. Thus, estrogen-sensitive POA efferents as well asnon-estrogen-sensitive LS efferents project to the AMY via the striaterminalis. Reductions in axonal excitability would inhibit neural conductionand transmission. Estrogen may therefore reduce the AMY inputs from the POA,without affecting those from the LS. Such alterations in the neural impulseflow may underlie estrogen-dependent neuroendocrine or behavioral regulation.