Effects of estrogen and aminergic drugs on thresholds of medial basal hypothalamic axons in the median eminence of the rat.
Antidromic responses were induced in the medial basal hypothalamus (MBH) of female rats by median eminence (ME) stimulation, and thresholds were measured under various endocrine conditions. Two different types of antidromic response were recognized. In 83 out of 97 responses, repetitive shocks to the ME at 20--40 Hz induced a fractionation of antidromically-driven spikes into A- and B-components. In the remainder, the antidromically activated spikes were stable to stimulation at high frequency. The threshold tended to show higher values in proestrus than in diestrus-I in both types of response. However, only in the former type of response, application of conditioning electrical shocks to the ME was effective in decreasing the threshold for successive test pulses. A decrease in the threshold lasted for 150--200 msec following the conditioning, with the lowest threshold at about 60 msec after the shock. Effects of the conditioning persisted in animals with chronic complete deafferentation of the MBH but were abolished in intact rats by reserpine treatment. Dopamine, but not norepinephrine or serotonin, mimicked the threshold-decreasing effect of the conditioning when applied to the ME. The results suggest the possibility of a depolarizing effect of some dopaminergic neural mechanism projecting from the MBH to the ME and acting on the axons of a particular type of MBH neuron characterized by fractionating spikes.
Effects of estrogen and aminergic drugs on thresholds of medial basal hypothalamic axons in the median eminence of the rat. Antidromic responses were induced in the medial basal hypothalamus (MBH) of female rats by median eminence (ME) stimulation, and thresholds were measured under various endocrine conditions. Two different types of antidromic response were recognized. In 83 out of 97 responses, repetitive shocks to the ME at 20--40 Hz induced a fractionation of antidromically-driven spikes into A- and B-components. In the remainder, the antidromically activated spikes were stable to stimulation at high frequency. The threshold tended to show higher values in proestrus than in diestrus-I in both types of response. However, only in the former type of response, application of conditioning electrical shocks to the ME was effective in decreasing the threshold for successive test pulses. A decrease in the threshold lasted for 150--200 msec following the conditioning, with the lowest threshold at about 60 msec after the shock. Effects of the conditioning persisted in animals with chronic complete deafferentation of the MBH but were abolished in intact rats by reserpine treatment. Dopamine, but not norepinephrine or serotonin, mimicked the threshold-decreasing effect of the conditioning when applied to the ME. The results suggest the possibility of a depolarizing effect of some dopaminergic neural mechanism projecting from the MBH to the ME and acting on the axons of a particular type of MBH neuron characterized by fractionating spikes.