The effects of handling, ether vapor anesthesia and blood sampling on serum LH and prolactin were determined in intact, castrate and dexamethasone-treated male rats. Cage removal and transport to an adjacent room increased LH and prolactin levels by 10 and 15 min after the initial animal disturbance. Intact male rats subjected to repeated ether anesthesia and blood sampling showed a more rapid increase in serum LH and prolactin than the preceding rats, since serum LH and prolactin was increased by 4, 8 and 15 min after initial cage disturbance. In a group of rats subjected to serial blood sampling over a longer time interval, both prolactin and LH levels remained higher than 90 min after initial animal handling. At 90 minutes after a single blood sampling, blood prolactin concentration remained higher than in controls. Serum LH levels returned to control levels 90 min after the stress of a single blood sampling. Although serum prolactin was increased in the castrate group subjected to serial anesthesia and blood sampling, LH concentrations were reduced under the same conditions. Injection of 5 and 50 mug of dexamethasone/100 g body wt for 8 days markedly reduced adrenocortical responsiveness to the stress of serial anesthesia and blood sampling at 1, 4, 8 and 15 min after initial rat disturbance. The 50 mug dexamethasone treatment reduced the stress-stimulated increase in serum prolactin at all blood sampling intervals. The dexamethasone-treated groups also showed smaller increases in serum LH at 8 and 15 min after first animal handling than the control rats. These results indicate that serum LH and prolactin concentrations are consistently increased by acute stress in intact male rats, the duration of the stress stimulation of LH and prolactin is at least 90 min under the conditions of this study, serum LH levels of castrate male rats are decreased by acute stress and dexamethasone administration lowers stress stimulation of LH and prolactin release.

Serum concentrations of prolactin and biochemical estimates of impulse traffic in dopaminergic neurons (neuronal ‘activity’) were compared in rats on the second day of diestrus and in 12-day postpartum lactating rats that were either suckled or were nonsuckled (pup-deprived). Indices of the activities of tuberoinfundibular, tuberohypophyseal and nigrostriatal dopamine (DA) neurons were obtained by measuring the α-methyltyrosine-induced decline of DA concentrations, and the accumulation of dihydroxyphenylalanine (dopa) after the administration of an inhibitor of aromatic L-amino-acid decarboxylase in the median eminence, posterior pituitary and striatum, respectively. Biochemical indices of tuberoinfundibular DA neuronal activity and the content of DA in the anterior pituitary gland were lower in pup-deprived lactating rats than in diestrous controls, and were further reduced by suckling. These changes appeared to be specific for tuberoinfundibular DA neurons since biochemical estimates of tuberohypophyseal and nigrostriatal DA neuronal activity were the same in all three groups of animals. Following pup removal serum prolactin concentrations in the dam decreased to basal levels within 4 h and remained low for at least 72 h. The rate of dopa accumulation in the median eminence of lactating rats increased 4 h after pup removal, but remained significantly lower than diestrous values for 72 h. These results indicate that an acute suckling stimulus activates a neuronal circuit which causes a prompt decrease in tuberoinfundibular DA neuronal activity. This decrease may play a role in the suckling-induced increase in prolactin secretion. Independent of these acute changes, the ‘basal’ activity of tuberoinfundibular DA neurons is reduced in lactating rats. This decrease appears to result from the lack of responsiveness of these neurons to the stimulating actions of prolactin. This is supported by the fact that the rate of dopa accumulation in the median eminence was increased in diestrous animals 12 h after the intracerebroventricular injection of prolactin or 16 h after the administration of haloperidol (which increases serum prolactin concentrations) but these treatments were without effect in lactating animals. The decreased responsiveness of tuberoinfundibular DA neurons in lactating rats to prolactin may contribute to the ability of the anterior pituitary gland in these animals to maintain a high secretion rate of this hormone.

Results of previous studies have revealed that prolactin causes a delayed (12–16 h) increase in the rate of synthesis and turnover of dopamine (DA) in terminals of tuberoinfundibular (TI) neurons in the median eminence. Attempts to demonstrate a rapid in vivo action of prolactin on these neurons has been frustrated because pharmacological manipulations needed to make the biochemical measurements of TIDA neuronal activity (i.e., administration of α-methyl-tyrosine or NSD 1015) inhibit DA synthesis and thereby remove the tonic inhibitory control of DA on prolactin secretion. Thus, ‘control’ rates of synthesis and turnover of DA in terminals of TIDA neurons are actually values obtained in the presence of high circulating concentrations of prolactin. Results of the present in vivo studies demonstrate that there are two components to the activation of TIDA neurons by prolactin: a rapid ‘tonic’ component, which is responsive to acute changes in prolactin concentrations, and a delayed ‘induction’ component, which is activated by long-term changes in prolactin concentrations. Experimental observations which support this proposal are described below. Hypophysectomy or treatment with bromocriptine (a DA agonist) reduce circulating levels of prolactin and reduce the rate of DA synthesis in the median eminence. Intracerebroventricular (i.c.v.) administration of prolactin to these animals increases the rate of DA synthesis in the median eminence within 4 h (rapid ‘tonic’ component) and then causes a further increase after 12 h (delayed ‘induction’ component); only the latter component is blocked by treatment with cycloheximide, indicating the involvement in protein synthesis. In addition, the delayed ‘induction’ component of the feedback activation of TIDA neurons represents a change in the capacity of the rapid ‘tonic’ component since the delayed effect is observed only if the TIDA neurons are exposed to prolactin for a brief period prior to the time that measurements of DA synthesis rates are made. This is exemplified by the fact that the increased rate of DA synthesis in the median eminence observed after circulating concentrations of prolactin have been elevated for 16 h by the administration of a large dose of haloperidol (1 mg/kg) can be prevented if the prolactin levels are reduced by bromocriptine 4 h prior to measurement. In turn, this action of bromocriptine can be reversed by the i.c.v. administration of prolactin 4 h prior to measurement. Furthermore, a low dose of haloperidol (0.1 mg/kg), which increases prolactin at 1 h but not at 16 h, does not increase DA synthesis in the median eminence at 16 h (delayed component). However, if a second injection of this same low dose of haloperidol is administered at 12 h, the rate of DA synthesis at 16 h is increased to the same degree as the larger dose of the DA antagonist. Thus, at any point in time, the activity of TIDA neurons appears to be influenced by the circulating concentration of prolactin at the time of measurement (rapid ‘tonic’ component) and by the previous p...

The effect of chronic stress on adrenocorticalfunction was tested in young and aged male and female rats. The rats were subjected twice a day to 2 h restraint stress for 20 days. Adrenocortical responsiveness to stressors was decreased during the treatment in all groups. Responsiveness to ACTH injection was greater than stress responsiveness in all groups. The decrease in stress responsiveness was greater in the young than in the aged groups. The data suggest that elevated corticosterone concentrations from chronic stress adrenocortical activation result in incomplete feedback inhibition of the adrenocortical control mechanism. The increased inhibition in the young groups supports the concept of decreased adrenocortical control system sensitivity in the aged animal.