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The precise role played by serotonin (5-HT) in taste--an issue of great interest given the involvement of serotonin in human sensory and eating disorders--is a matter of considerable debate, perhaps because of the variety of methodologies that have been brought to bear by different researchers. Here, we use multiple methods to reveal the motivational mechanism whereby 5-HT(1A) receptor activation modulates drinking behavior. Subcutaneous injections of the selective 5-HT(1A) agonist 8-hydroxy-2-di-n-propylamino-tetralin (8-OH-DPAT), a drug that reduces 5-HT release by acting on presynaptic autoreceptors, dose-dependently increased consumption of 0.45 M NaCl in a one-bottle test. In a two-bottle test, however, 8-OH-DPAT-treated animals (30 microg/kg/ml) demonstrated decreased NaCl preference--although our detection of this effect was obscured by adaptation to the drug across days. Rats' performance in a brief access test confirmed that 8-OH-DPAT decreased preference for saline by both increasing water consumption and decreasing NaCl consumption. Finally, taste reactivity tests demonstrated that the latter result does not reflect decreased NaCl palatability. Overall, the results suggest that 8-OH-DPAT-induced 5-HT hypofunction increases thirst without substantially affecting the palatability of NaCl.

Investigating the motivational mechanism of altered saline consumption following 5-HT1a manipulation.