Hideo NegoroRobert C. HollandMahidol University2018-03-122018-03-121972-07-20Brain Research. Vol.42, No.2 (1972), 385-402000689932-s2.0-0015517464https://repository.li.mahidol.ac.th/handle/123456789/9999The activity of 202 units in the paraventricular nucleus (PVN), identified by antidromic activation of the neurohypophysis, was studied during and after single shock or train stimulation. After a single shock at 20% above threshold intensity there was a mean period of 54.7 msec of inhibition of spontaneous firing. Increasing the intensity increased the duration of the inhibitory period until an upper limit, depending upon the neurone, was reached. Train stimulation of 5 sec was followed by several seconds of inhibition. The duration of inhibition was longer if the intensity or frequency of the stimuli in the train was increased. Under these conditions the B (SD) potential was lost early in the train and only the A (IS) potential followed each stimulus. It is suggested that recurrent inhibition at the soma accounts for the loss of the B potential and the post-stimulation period of inhibition of spontaneous firing and that the inhibition is cumulative. Although presynaptic inhibition of PVN afferents cannot be excluded, we could find no evidence for this type of inhibition in PVN. After a period of fast spontaneous discharge or an antidromic train, the refractory period was lengthened and the threshold for antidromic activation was elevated. Hyperpolarizing afterpotentials are very likely the basis for these changes in the properties of the neurone and account at least in part for the gradual lengthening of the latency of the antidromic response observed with longer trains of up to 60 sec. The results suggest that within the PVN is a mechanism which would provide for release of oxytocin in a phasic manner in spite of continuing activity in excitatory afferents to the PVN. © 1972.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyMedicineNeuroscienceInhibition of unit activity in the hypothalamic paraventricular nucleus following antidromic activationArticleSCOPUS10.1016/0006-8993(72)90538-0