LATERAL VENTRICULAR INJECTIONS OF THE NK3 AGONIST SENKTIDE AFFECT SALT TASTE-ELICITED RESPONSES

Central injections of the selective tachykinin NK3 receptor agonist se nktide (SENK) suppresses salt appetite. Also, following SENK, intraora l infusions of hypertonic NaCl elicit fewer ingestive taste reactivity responses and more aversive responses than following intraventricular injections of isotonic saline. This pattern of taste reactivity resul ts suggest that SENK affects the oral stimulating properties of salt t aste. Before accepting this interpretation, however, alternative expla nations need to be examined. The following experiments evaluated wheth er the effects of intraventricular SENK injection on taste reactivity could be due to: 1) a general oral motor impairment that reduces inges tive responding to tastes (Experiment 1) or; 2) SENK having aversive c onsequences (Experiment 2). In Experiment 1, the effects of intraventr icular injections of SENK (200 ng) on taste reactivity responses to 0. 5 M NaCl and 0.1 M sucrose were measured in sodium deficient rats. Int raoral infusions of 0.5 M NaCl elicited fewer ingestive taste reactivi ty responses following SENK than injections of isotonic saline in sodi um deficient rats. Sucrose continued to elicit the same high number of ingestive taste reactivity responses following intraventricular injec tions of isotonic saline and SENK. Thus, SENK did not cause a general decrease in ingestive responding. A conditioned taste aversion test wa s employed in Experiment 2 to determine if SENK had aversive consequen ces. Rats were given 30 min access to alanine (0.3 M) and were then ad ministered either lithium chloride (LiCl) or intraventricular injectio ns of SENK (200 ng) on three consecutive days. Rats avoided alanine th at was paired with LiCl, but those rats that had alanine paired with S ENK showed no avoidance of the taste even after three pairings. These results replicate findings that intraventricular injections of the NK3 agonist SENK decreases the palatability of NaCl (as measured by taste reactivity) and suggest that its effect on NaCl-elicited taste reacti vity is not due to the treatment causing a motor impairment or malaise . (C) 1998 Elsevier Science Inc.