ACUTE RESTRAINT STRESS DECREASES DOPAMINE SYNTHESIS AND TURNOVER IN THE MEDIAN-EMINENCE - A MODEL FOR THE STUDY OF THE INHIBITORY NEURONAL INFLUENCES ON TUBEROINFUNDIBULAR DOPAMINERGIC-NEURONS

The effects of acute stress on serum prolactin concentrations and tuberoinfundibular dopaminergic (TIDA) neuronal activity were studied in female rats. TIDA neuronal activity was estimated by measuring the rate of dihydroxyphenylalanine (DOPA) accumulation after the administration of a decarboxylase inhibitor (NSD 1015) and the rate of decline of dopamine (DA) after the administration of a tyrosine hydroxylase inhibitor (.alpha.-methyltyrosine) in the median eminence. Serum prolactin concentrations were increased following 30 min of supine immobilization (restraint stress), but returned to control levels by 2,8, and 16 h after the onset of this stress. The rate of DOPA accumulation was decreased during the 30 min of restraint; it was still further reduced 2 h later but had returned to control levels 8 and 16 h later. No change in the rate of DOPA accumulation was observed in the striatum or neurointermediate lobe of the pituitary at any time after the start of restraint. Restraint stress also decreased the rate of DA turnover in the median eminence, but was without effect on the rates of DA turnover in the striatum or neurointermiediate lobe. These results suggest that restraint stress activates an inhibitory neuronal pathway which decreases the activity of TIDA neurons and may be responsible, at least in part, for the increase in serum prolactin concentrations. The responsiveness of TIDA neurons to the stress-induced decrease in activity was not influenced by the time of day or the stage of the estrous cycle. Not all stressful manipulations decreased TIDA neuronal activity. While 30 min of restraint, swimming, novel environment and ether-vapor stresses increased serum prolactin concentrations, only restraint and seim stress decreased TIDA neuronal activity. Restraint stress was also effective in decreasing the activity of TIDA neurons which had been simulated by pretreatments which increased circulating prolactin concentrations (haloperidol, ovine prolactin). The stress-induced increase in serum prolactin and the decreased in TIDA neuronal activity were both blocked by 5-hydroxytryptamine (5HT) antagonists (metergoline and cinanserin) and by muscarinic cholinergic antagonists (atropine and scopolamine). Opiate antagonists (naloxone and naltrexone) were without effect on the stress-induced changes in serum prolactin concentrations and TIDA neuronal activity. The results suggest that 5HT and cholinergic neuronal systems play a role in the stress-induced increase in serum prolactin concentrations and the decrease in TIDA neuronal activity.