Dopamine Regulation of Swim Stress Induction of the Pituitary Intermediate Lobe Proopiomelanocortin System

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Abstract
Previous studies have indicated that 30 min of swimming in room temperature water is a potent stimulus for the secretion of β-endorphin (βE) from the intermediate lobe (IL) of the pituitary in rodents. Repeated daily challenge with this paradigm over days to weeks leads to a progressive increase in proopiomelanocortin (POMC)-derived IL peptides and POMC mRNA levels as well as an increase in the stimulated secretion of βE in response to rechallenge with swim. The current studies were undertaken to examine the possible role of dopamine systems in mediating swim stress-induced changes in IL βE biosynthesis and release. Confirming previous results, a 30 min swim stress exposure caused plasma concentrations of βE to increase several fold. Apomorphine (APO), a dopaminergic agonist, completely blocked this effect, suggesting that dopamine receptors may mediate the acute IL response to swim stress. Animals that swam once daily for 14 days displayed elevated βE levels in both the IL and plasma 24 h after the last swim session. In these animals, repeated administration of APO did not reverse swim-stress-induced changes in βE. Immediately following an acute-swim rechallenge, animals which had been previously swim-stressed for 14 days demonstrated significantly greater βE release than naive animals. Again, an acute injection of APO inhibited the acute increase in IL secretion, suggesting that repeatedly swum animals are still responsive to the acute effects of APO even though repeated coadministration of APO with swim exposure had no effect on IL βE peptide stores or plasma βE concentration. In a final experiment, animals treated for 14 days with either daily swim stress or a maximally effective dose of haloperidol (a dopaminergic antagonist) displayed increased IL levels of POMC mRNA. Combined haloperidol and swim treatment had an additive effect on POMC mRNA levels, suggesting that swim stress might be acting via nondopaminergic mechanisms. Taken together, these studies indicate that chronic swim-stress-induced changes in IL βE biosynthesis and secretion may involve non-dopaminergic systems.

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