The regulation of prolactin secretion by tuberoinfundibular dopamine (DA) neurons appears to be altered in the aged rat: the concentration of prolactin in the serum increases and the activity of the tuberoinfundibular DA neurons decreases. In the young female rat a brief period of stress reduces the tuberoinfundibular DA neurosecretory activity and increases the secretion of prolactin. The purpose of the present study was to determine if the responsiveness of tuberoinfundibular DA neurons to restraint stress is altered in the aged female rat. The activity of these neurons was estimated from the rate of DA synthesis in their terminals in the median eminence, as measured by the rate of accumulation of dihydroxy-phenylalanine (DOPA) after the administration of a decarboxylase inhibitor. Thirty minutes of restraint stress increased serum prolactin concentrations in both young (3 months) and aged (26 months) constant estrous rats, but reduced the rate of DOPA accumulation in the median eminence of only the young rats. Restraint also decreased the rate of DOPA accumulation in the median eminence of intermediate-aged rats (14 months) independently of whether the rats were exhibiting normal ovarian cycles (measured on the day of estrus) or were in a constant estrus. This suggests that the loss of ovarian cyclicity per se is not associated with the age-related change in the response of tuberoinfundibular DA neurons to restraint stress. To determine if the lack of response of tuberoinfundibular DA neurons to stress is related to the reduced basal activity of these neurons in the aged rat, the response of tuberoinfundibular DA neurons to 30 min of restraint was determined in rats that were pretreated with haloperidol. Haloperidol increased serum prolactin levels and consequently the tuberoinfundibular DA neuronal activity in both young and aged rats, but restraint stress reduced the rate of DOPA accumulation only in the young rats. These results reveal that the inhibition of tuberoinfundibular DA neurons by stress is impaired in the aged rat and suggest that the inhibitory neuronal mechanisms that mediate this response become disrupted as the female rat ages.