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Castration in the rat significantly lengthened the refractory period of medial preoptic–anterior hypothalamic neurones with outputs into the medial forebrain bundle but not of those with outputs to the lateral septum. Treatment with testosterone propionate reduced the neuronal refractory period to its lowest level at the same time as it restored mounts and intromissions (after 5 days). Equally, when treatment was ended at 15 days, mounts and intromissions were no longer shown when the refractory period lengthened again 14 days later. The sub-population of neurones which also received inputs from the contralateral fimbria (through the corticomedial amygdala) showed the same results as the overall population. Castration also significantly increased the baseline firing rates of medial preoptic–anterior hypothalamic neurones receiving inputs from the medial forebrain bundle. The same effect was observed for the sub-population of neurones which also had inputs from the contralateral fimbria, but castration significantly reduced the percentage of neurones responding to this additional input. The neurones having inputs with the fastest conduction velocity were responsible for these changes in firing rate and the input neurones were therefore probably non-dopaminergic.