Abstract
Stimulation of the median eminence of female rats inhibited the spontaneous firing of antidromically identified tubero-infundibular units. Some units could be inhibited by stimuli subthreshold for the antidromic spike. A conditioning stimulus of subthreshold intensity for the antidromic spike also delayed or abolished the invasion of the soma and dendrites of the same unit by antidromic action potentials evoked by a suprathreshold stimulus given 2-10 ms later. Although strychnine (0.2 mg/kg, i.v.) did not significantly alter the inhibition evoked by stimulation of the median eminence, it was abolished by picrotoxin (2-6 mg/kg, i.v.). In 7 of the 57 identified units examined stimulation of the median eminence facilitated the spontaneous firing. After an i.v. injection of picrotoxin the facilitatory response was observed in 37 of the 46 units tested. Post-stimulus time histograms obtained from the same unit before and after an injection of picrotoxin demonstrated that the latency and duration of the facilitation did not always coincide with that of the inhibition. After an injection of picrotoxin the field potential evoked by antidromic stimulation of the median eminence consisted of a small positive wave followed by a negative wave. Frequently the negative wave of the field potential was accompanied by a convulsive discharge. The latency of the negative wave appears to be identical to that of the facilitation seen in nearby single units. The facilitation evoked by antidromic stimulation in the presence of picrotoxin was blocked by an i.v. injection of .alpha.-methyl-p-tyrosine (250 or 375 mg/kg). None of the 9 units sampled from rats pre-treated with .alpha.-methyl-p-tyrosine injected twice i.p. (250 mg/kg for each) were facilitated by stimulation of the median eminence following i.v. picrotoxin, while 8 of the 11 units sampled from control rats pre-treated with L-tyrosine could be facilitated by antidromic stimulation. Tubero-infundibular neurosecretory neurons may be inhibited and facilitated by neural pathways which could involve the axon collaterals of the neurosecretory neurons which project to the external layer of the median eminence. GABA-releasing neurons may mediate the inhibition, and catecholaminergic neurons may be involved in the facilitatory pathways. Presumably the facilitation is normally masked by the activity of the GABA-releasing neurons.