Perceptual characteristics of the amiloride-suppressed sodium chloride taste response in the rat.

Assessed the contribution of amiloride-sensitive membrane components to the perception of NaCl taste using a conditioned taste aversion procedure with 8 groups of adult rats conditioned to avoid either 0.1M NaCl, 0.5M NaCl, 0.1M NH?Cl, or 1.0M sucrose while their tongues were exposed either to water or to amiloride hydrochloride. Differences in the acquisition of taste aversions between the amiloride- and nonamiloride-treated groups were not apparent when the conditioned stimulus (CS) was 0.5M NaCl, 0.1M NH?Cl, or 1.0M sucrose. Although the magnitude of the 0.5M NaCl aversion was similar between amiloride- and nonamiloride-treated Ss, the perceptual characteristics of the CS differed between groups. Amiloride-treated Ss avoided monochloride salts after conditioning to 0.5M NaCl but not nonsodium salts or nonsalt stimuli. Ss not treated with amiloride only generalized the 0.5M NaCl aversion to sodium salts. The "salty" taste of NaCl is related to the amiloride-sensitive portion of the functional taste response in rats. The portion of the NaCl response insensitive to amiloride has "sour-salty" perceptual characteristics and is not perceived as being salty. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Anion Size Does Not Compromise Sodium Recognition by Rats After Acute Sodium Depletion.

Amiloride-insensitive sodium taste transduction is severely limited by large anions (i.e., gluconate). We found that in a brief-access taste test, sodium-depleted rats exhibited similar levels of increased licking to several sodium salts regardless of anion but did not increase licking to nonsodium salts compared with water. The enhanced licking of sodium salts was abolished in the presence of amiloride. These results suggest that the amiloride-sensitive taste transduction pathway is not only necessary but that it is also sufficient for sodium identification in rats. Sodium-depleted rats tested with amiloride initiated significantly more trials than nondepleted rats; hence, appetitive behavior was mildly potentiated by depletion, even in the absence of a sodium taste cue. Overall, these findings provide compelling support for the primacy of the amiloride-sensitive taste transduction mechanism and its associated neural pathway in the recognition of the sodium cation. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lesions of the gustatory neocortex on taste aversion learning in the rat.

In 5 experiments, 110 normal male Long-Evans hooded rats and 125 Ss with lesions of the gustatory neocortex (GN) were compared for their ability to learn aversions to taste cues paired with toxicosis. When the taste presentation was followed immediately by toxicosis, normal Ss and 8 Ss with lesions of the posterior (visual) neocortex learned aversions to sucrose, sodium chloride, quinine hydrochloride, and hydrochloric acid solutions. Ss with GN lesions learned aversions to all solutions except sucrose. In preference tests, all solutions were shown to be discriminable from water by both normal and GN-lesioned Ss. Under conditions in which a 6-hr delay separated taste presentation and toxicosis, normals again learned specific aversions to all 4 solutions, but Ss with GN lesions failed to learn specific aversions to sucrose, sodium chloride, and hydrochloric acid solutions. It was shown that the ability of Ss with GN lesions to learn aversions to sucrose and quinine depended on stimulus concentration. It is proposed that the data can be accounted for by postulating a change in the threshold for taste illness associations following GN lesions. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste as a dipsogenic stimulus.

Studied solution drinking in 50 male, nondeprived, Sprague-Dawley albino rats to determine how much animals will drink for reasons of taste alone. 4 different taste stimuli (sucrose, glucose, sodium saccharin, and sodium chloride) were used, each covering a wide range of concentrations. The same Ss were then retested after 16 hr. of water deprivation, and intakes under deprived and nondeprived conditions were compared. Results show that Ss ingested large volumes of sweet solutions in the absence of any need, and that water deprivation added only a small increment to the already high intakes of sweet solutions. Sodium chloride solutions, on the other hand, were ingested in relatively small quantities by nondeprived Ss, but water deprivation produced a large increase in intake. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sodium depletion enhances salt palatability in rats.

Stereotyped fixed action patterns (FAPs) elicited in rats by oral infusions of taste solutions can be classified as either ingestive or aversive. They reflect the palatability of the taste and can be modified by learning and by the physiological state of the animal. The present 2 experiments, with 5 male Sprague-Dawley rats, demonstrated that when the physiological state of the S was altered by sodium depletion, the pattern of FAPs elicited by oral infusions of 0.5 M NaCl shifted from a mixture of ingestive and aversive components (while sodium replete) to exclusively ingestive ones (while sodium deplete). This shift in taste reactivity occurred the 1st time the Ss were made sodium deplete. A similar shift did not accompany infusions of 0.01 M HCl, a taste solution that also elicited mixed ingestive and aversive FAPs. This result suggests that the shift in response to NaCl was not due to a general change in ingestive bias or to a general taste deficit. On the basis of the change in FAPs, it is concluded that the palatability of highly concentrated salt solutions increases in sodium-deplete rats. Such a shift in salt palatability may be instrumental in directing the appetitive behavior of the animal. (33 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Absence of differential associative responses to novel and familiar taste stimuli in rats lacking gustatory neocortex.

24 Long-Evans hooded rats lacking gustatory neocortex and 24 normal rats were familiarized to either hydrochloric acid or quinine hydrochloride solutions during free-drinking trials. Ss were subsequently trained to avoid either the familiar or the novel taste stimulus, using a balanced design, by pairing the to-be-associated taste with ip injections of apomorphine hydrochloride. Balanced, nonpaired presentations of the other taste solution and water were also presented. Normal Ss learned to avoid the novel taste more efficiently than the familiar taste. Ss with gustatory neocortex lesions did not differentiate novel from familiar tastes. They learned aversions to both in a manner highly similar to the aversion learning of familiar tastes by the normal group. Therefore, results demonstrate that Ss lacking gustatory neocortex displayed an associative deficiency only when they were trained on novel stimuli. This suggests that gustatory neocortex lesions disrupt the conditionability of taste stimuli by reducing or eliminating responses to taste novelty. This interpretation is supported by the absence of a "neophobic" response in the lesioned rats to the first presentation of a taste stimulus. (26 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Heredity and experience: Their relative importance in the development of taste preference in man.

Heritability estimates for sucrose, lactose, and sodium chloride taste preferences were uniformly low in a total of 311 pairs of monozygotic and like-sex dizygotic twins between 9 and 15 yrs of age. Black Ss preferred more concentrated solutions of all 3 tastants than did Caucasian Ss. This effect was independent of socioeconomic status in the total sample. Males preferred more concentrated solutions of sucrose and lactose than did females, but there were no sex differences in sodium chloride preference. The possibility that early intake experiences may play a role in the determination of enduring taste preferences in humans is discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Failure of sodium- and calcium-deficient rats to acquire conditioned taste aversions to the object of their specific hunger.

Attempted to condition taste aversions to the objects of 2 mineral-specific hungers in 2 experiments with a total of 116 male Sprague-Dawley rats. Both the innate preference of adrenalectomized Ss for sodium and the learned preference of parathyroidectomized Ss for calcium were studied. None of the sodium-deficient Ss poisoned after drinking NaCl reached a taste-avoidance criterion, even after 9 pairings of salt ingestion with aversive lithium chloride injections. 6 of 11 calcium-deficient Ss did not meet the salt-avoidance criterion after 10 pairings. Nondeficient control Ss learned to avoid these salt solutions completely after an average of only 3 such pairings. Besides unmasking a surprising degree of similarity between the learned and innate specific hungers studied, results clearly demonstrate a powerful influence of physiological need on aversion conditioning. (38 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Within-compound learning with US presentation in taste aversion.

Determined whether the presentation of a LiCl unconditioned stimulus/stimuli (UCS) disrupts within-compound learning in a taste aversion preparation, using 30 male and 32 female rats in 3 experiments. In Exp I, Ss showed stronger associations between 2 solutions presented in a compound when the compound was followed by LiCl. Exp II showed that an immediate LiCl injection produced stronger flavor–flavor association than a delayed injection. Exp III provided a comparison with Ss that did not receive the treatment to enhance consumption of salty solutions. Results indicate that the effects of Exp II depended on the treatment that altered consumption of 1 component. (French abstract) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste potentiation of auditory aversions in rats (Rattus norvegicus): A case for spatial contiguity.

Examined whether an auditory stimulus, which is not likely to be associated with food in rats, could be potentiated by taste and whether spatial contiguity is a necessary requirement for this effect. Ss were 13 male and 42 female Sprague-Dawley rats. An aversion for an auditory stimulus was established in Ss when a tone was spatially and temporally contiguous with a novel taste in a food CS compound followed by toxicosis. The procedure involved varying the location of the tone relative to a novel-tasting food. During toxicosis conditioning, 1 group ate sweet food with a speaker located in the food, 2 groups ate sweet food with the speaker displaced (near or far) from the food, and a 4th group was presented with a tone without food available. It was found that the potentiation of auditory aversions required both the presence of a novel taste and spatial contiguity between the taste and the tone. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Flavor-illness aversions: Gustatory neocortex ablations disrupt taste but not taste-potentiated odor cues.

Two studies evaluated the contribution of the gustatory neocortex (GN) to the potentiation of odor by taste during illness-induced aversions in 130 male Sprague-Dawley rats. In Exp I, Ss lacking GN and controls were given an odor, a taste, or an odor–taste compound cue followed by intragastric gavage of LiCl. Prior to conditioning, neophobia for flavored solutions was absent in Ss with GN lesions. After pairing with LiCl, GN Ss developed normal conditioned odor aversions, whereas conditioned taste aversions were attenuated or totally blocked. Potentiation of odor by taste after compound conditioning was evident in both control and GN Ss. In Exp II, normal Ss were given compound conditioning to induce potentiated odor aversions and then given GN lesions prior to tests with the odor and taste components. Taste aversion retention was totally disrupted by GN ablation; potentiated odor aversions were retained by both groups, although the GN group extinguished faster. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Neonatal ablations of the gustatory neocortex in the rat: Taste aversion learning and taste reactivity.

Sprague-Dawley rats sustaining ablations of gustatory neocortex (GN) at 2, 10, 20, or 60 days of age were compared with control-lesion and anesthetized controls (N?=?151) in the acquisition and extinction of a learned taste aversion. Ss were also tested for taste preference across 5 concentrations of NaCl solution (.04, .08, .15, .3, and .6 M). Results indicate that GN ablation disrupted aversion acquisition and extinction regardless of age at surgery. Taste-response functions for solutions shown by all GN Ss mirrored those of controls: preference (relative to water baseline) for middle concentrations and rejection of the strongest concentration. It is suggested that the 20- and 60-day-old GN Ss were hyperresponsive to the suprathreshold concentrations of NaCl (excepting the .6-M concentration). The increased response to NaCl in 20- and 60-day-old GN Ss may have been related to the significant decreases in water consumption relative to that of controls. Water consumption of controls and GN Ss in 2- and 10-day-olds was essentially equal. It is concluded that infant ablation of the GN does not spare normal taste aversion learning and that rats with GN ablations, regardless of age at surgery, respond in a normal manner to the hedonic aspects of NaCl solutions. (22 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Evidence for a learning component of sodium hunger in rats.

Used acute esophageal-fistula albino Wistar rats with stomach catheters to separate the roles of taste and feedback in sodium hunger. Of 294 fistulated rats put into the test cages, 171 provided usable data. The effects of sodium deficiency (D; dialysis with glucose) vs. nondeficiency (D; dialysis with saline) were observed on drinking of water and of saline (4 real-drinking, nonoperated groups). These same factors plus the effects of intragastric injection of water or saline (8 groups) were investigated in sham drinkers. Results indicate that (a) the initial positive response to saline by deficient Ss did not appear in acute sham drinkers whether sodium feedback occurred or not; (b) in the later portions of the 12-hr test, a need-related response appeared that seemed to be based on feedback. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Bait shyness: Avoidance of the taste without escape from the illness in rats.

Conducted 3 experiments with 50 young adult Sprague-Dawley rats. Thirsty Ss habituated to drinking .12 M sodium chloride accepted .12 M lithium chloride for 5 min on the 1st trial but stopped short of their sodium baseline. With repeated trials they reduced consumption of the toxin by either (a) detecting subtle oral CS differences, thus avoiding toxicosis (UCS) or (b) detecting earlier signs of malaise (UCS), thus escaping further distress. When both solutions were masked with saccharin, discrimination was more difficult but still possible. When both solutions were mixed in a solution masking all 4 taste qualities, discrimination was severely disrupted. When oral sensors were bypassed with nasopharyngeal tubes, intragastric pumping Ss were unable to use postingestional cues to escape, even though such cues were proximal to the ultimate malaise. Oral cues at the distal end of the consummatory chain were extremely effective. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of dietary NaCl deprivation during early development on behavioral and neurophysiological taste responses.

Investigated whether the gustatory system can be modified by restricting dietary NaCl during early development by recording neurophysiological taste responses in Sprague-Dawley rats at various times after deprivation (Exp I), and by measuring behavioral taste preferences in 3 groups of 7 NaCl deprived adult rats (Exp II). Overall findings indicate that Ss deprived of dietary NaCl from the 3rd day of gestation to 12 days postnatally and then placed on a NaCl-replete diet had chorda tympani nerve responses similar to those of nondeprived Ss when recordings were made at 28 days of age and older; however, preferences for NaCl solutions over water were significantly less than those of controls when tested at adulthood. NaCl deprivation in Ss from the 3rd day of gestation to approximately 35 days postnatally resulted in altered chorda tympani nerve responses to NaCl but not to other stimuli such as NH?Cl and KCl. Thus, it is concluded that restriction of dietary NaCl at a period in the rat's development when peripheral and central taste responses are changing results in short-term alterations in peripheral neural responses and in long-term changes in preference behaviors. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of potassium depletion on mineral appetite in the rat.

Studied potassium appetite in normal female Sprague-Dawley rats and in rats in which the total body potassium had been reduced by 15-20%. Potassium depletion resulted in increased ingestion of solutions of NaCl, KCl, CaCl2, and quinine sulphate in concentrations that were unacceptable to normal Ss. The amount of potassium ingested was related to the degree of potassium depletion and repletion was usually completed within 24 hr. when potassium was offered. Potassium-depleted Ss also drank large quantities of aversive concentrations of sodium chloride. This was preferred to potassium chloride and its ingestion appeared to be unrelated to need. The appetite state was reversed by prior intragastric repletion with potassium but not with sodium salts. (19 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of basolateral amygdala lesions on neophobia, learned taste aversions, and sodium appetite in rats.

Reports results of 8 experiments with a total of 327 male Sprague-Dawley rats. Lesions to the basolateral amygdala produced permanent impairment in Ss' ability to learn a taste aversion. When lesions were administered after Ss had already learned an aversion, there was complete loss of the aversion. Ss with amygdala lesions also had a diminished neophobic response when presented with a novel solution and showed a more generalized aversion to water after a sucrose-sickness trial. Whether a solution was novel or familiar affected the learning of an aversion for controls more than it did for Ss with amygdala lesions. Ss with amygdala damage also showed less sodium appetite than normals in response to desoxycorticosterone acetate injections. These results indicate that rats with amygdala lesions have deficits in recognizing the significance of stimuli. (49 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste reactivity as a dependent measure of the rapid formation of conditioned taste aversion: A tool for the neural analysis of taste-visceral associations.

Investigated the ability of animals to form taste aversions following neural manipulations. In Exp 1, 10 rats received intraoral infusions of sucrose every 5 min starting immediately after the injection of LiCl. 12 controls were injected with NaCl. Oromotor and somatic taste reactivity behaviors were videotaped and analyzed. Lithium-injected Ss decreased their ingestive taste reactivity over time; aversive behavior increased. Controls maintained high levels of ingestive responding and demonstrated virtually no aversive behavior following sodium injection. Ss were tested several days later for a conditioned taste aversion (CTA). Rats previously injected with lithium demonstrated significantly more aversive behavior than controls. Exp 3 revealed that when similarly treated rats were tested for a CTA while in a lithium-induced state, difference in the ingestive behavior was observed. In Exp 2, naive rats were injected with NaCl or LiCl but did not receive their 1st sucrose infusion for 20 min. Ss also received infusions at 25 and 30 min postinjection. There were no differences in the task reactivity behavior displayed. Rats dramatically changed their oromotor responses to sucrose during the period following LiCl administration, provided the infusions started immediately after injection, a change attributable to associative processes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Disruption of conditioned taste aversion in the rat by stimulation of amygdala: A conditioning effect, not amnesia.

Conducted 2 experiments with a total of 143 male Wistar rats to determine whether the disruption of conditioned taste aversion by amygdaloid brain stimulation (BST) during conditioning could be attributed to the stimulus properties of the BST. In Exp I, Ss receiving BST (a) while drinking saccharin, (b) during the onset of LiCl toxicosis, or (c) in the interval between taste exposure and toxicosis drank significantly more saccharin solution during a 48-hr retest than implanted or unoperated controls receiving similar taste–toxicosis pairings. In contrast, Ss receiving BST during both conditioning and retention trials developed a strong conditioned aversion. Exp II confirmed that BST formed a compound with the taste of the saccharin solution. A small but significant aversion was displayed by groups exposed to BST plus taste during conditioning and to either taste alone or BST alone during the retest. Again, the group presented with BST and taste prior to and following LiCl toxicosis displayed a strong conditioned aversion. Results suggest that disruption of conditioned taste aversion with amygdaloid BST represents a conditioning effect, not amnesia. (31 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Contribution of the rat's neocortex to ingestive control: I. Latent learning for the taste of sodium chloride.

Conducted 3 experiments with 13 decorticate and 12 control male Sprague-Dawley rats to investigate whether some permanent ingestive control deficit would be revealed in a latent learning paradigm for salt taste. The ability of Ss to associate how they obtained the taste of NaCl when Na-replete was assessed by examining barpresses during extinction when Na-depleted. Intact Ss exposed to 4–6 hrs of NaCl taste training retained the association after decortication; decorticate Ss exposed to the same training acquired the association. Decorticate Ss exposed to as little as 2 min of NaCl taste training demonstrated the ability to associate barpressing with NaCl by their resistance to extinction. This association was specific to NaCl training. It is concluded that subcortical structures are adequate for latent learning involving NaCl taste. Conversely, previous research has shown that the neocortex is required for the retention of taste-aversion learning for the same taste. (43 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)