Sucrose Licking Research Articles

The Selective Serotonin Reuptake Inhibitor Paroxetine Does Not Alter Consummatory Concentration-Dependent Licking of Prototypical Taste Stimuli by Rats

Serotonin and the 5HT(1A) receptor are expressed in a subset of taste receptor cells, and the 5HT(3) receptor is expressed on afferent fibers innervating taste buds. Exogenous administration of the selective serotonin reuptake inhibitor, paroxetine, has been shown to increase taste sensitivity to stimuli described by humans as sweet and bitter. Serotonergic agonists also decrease food and fluid intake, and it is possible that modulations of serotonin may alter taste-based hedonic responsiveness; alternatively, or in combination, serotonin may interact with physiological state to impact ingestive behavior. In this study, the unconditioned licking of prototypical taste stimuli by rats in brief-access taste tests was assessed following paroxetine administration (0.3-10 mg/kg intraperitoneal). We also measured sucrose licking by rats in different deprivation states after paroxetine (5 mg/kg). In neither experiment did we find any evidence of an effect of paroxetine on licking relative to water to any of the taste stimuli in the brief-access test at doses that decreased food intake. However, in some conditions, paroxetine decreased trials initiated to tastants. Therefore, a systemic increase in serotonin via paroxetine administration can decrease appetitive behavior in brief-access tests but is insufficient to alter taste-guided consummatory behavior.

The inhibitory potency of SCH 23390 and raclopride on licking for sucrose increases across brief-access tests

There is extensive pharmacological and microdialysis evidence that central dopamine mechanisms are important for the mediation of the rewarding and reinforcing functions of sweet taste. One aspect of the pharmacological evidence for dopaminergic mediation of sweet reward is unclear. That is the positive interactive effect of ingestive experience and DA antagonist treatment reported by Wise and his colleagues in 1978 [1]. They showed that the inhibitory potency of pimozide increased over repetitive tests of saccharin (0.1%) ingestion. When pimozide was given before 8 daily, 10-minute tests in rats licking [2] or lever pressing [3] for 32% sucrose, however, the inhibitory effect of pimozide did not increase across tests. To reinvestigate the problem, we used a computer-assisted, repetitive, brief-access technique [4, 5] in which 10 male, non-deprived, Sprague Dawley rats licked 0.5 M sucrose for 60 s in four trials with a 30-second intertrial interval. Thirty minutes before the first trial, each rat received an ip injection of the D1 antagonist SCH 23390, the D2/3 antagonist raclopride, or vehicle. SCH 23390 and raclopride decreased licking significantly, their inhibitory effects increased significantly within and across the 4 trials, and the temporal pattern of their inhibitory effects on latencies, and on cumulative and total licks was different. Thus we confirm an increase of the inhibitory potency of DA antagonists across ingestive tests and show for the first time that the interaction differs between D1 and D2/3 antagonists.

Parabrachial Y1/Y4 receptor stimulation increases licking for sucrose

Parabrachial Y1/Y4 receptor stimulation increases licking for sucrose

Roux-en-Y gastric bypass in rats increases sucrose licking depending on deprivation state and trial taking in brief access tests

Roux-en-Y gastric bypass in rats increases sucrose licking depending on deprivation state and trial taking in brief access tests

Dopamine on D2-like receptors is involved in reward evaluation in water-deprived rats licking for NaCl and water

The analysis of licking microstructure provides measures, size and number of licking bouts, which might reveal, respectively, reward evaluation and behavioural activation. Based on the ability of the dopamine D2-like receptor antagonist raclopride to reduce bout size and to induce an “extinction mimicry effect” on bout number, we suggested that the level of activation of reward-associated responses is updated, or “reboosted”, on the basis of a dopamine D2-like receptor-mediated evaluation process occurring during the consummatory transaction with the reward. Here we investigate the effects of the dopamine D2-like receptor antagonist raclopride (0, 25, 125, and 250 µg/kg) on the microstructure of licking for water and sodium chloride solutions (0.075 M, 0.15 M, and 0.3 M) in 12 h water-deprived rats. In each session, rats were exposed to brief contact tests (1 min) for each solution. Bout size, but not bout number, was decreased at the highest NaCl concentration. Raclopride reduced lick number owing to reduced bout size, while bout number was either not affected or even increased depending on the dose. These results are in agreement with the previous observations on sucrose licking, and suggest the involvement of dopamine D2-like receptors in an evaluation process occurring during the consummatory transaction with the reward.

A pause in nucleus accumbens neuron firing is required to initiate and maintain feeding.

Nucleus accumbens (NAc) inactivation increases food intake, indicating that NAc neurons exert ongoing inhibition of feeding. We previously described a subpopulation of NAc neurons that pause during sucrose licking and proposed that the pause permits consumption. We tested this hypothesis by first recording NAc neurons during sucrose consumption, and then electrically stimulating through the same electrodes. A large proportion of NAc shell and core neurons were inhibited during sucrose consumption, and local electrical stimulation abruptly interrupted licking. Effective stimulation sites were more anterior than ineffective sites in NAc. At low stimulus intensities, licking resumed immediately on stimulation offset. The latency to lick resumption from NAc neuron inhibition onset ( approximately 460 ms) was very similar to that after electrical stimulation offset ( approximately 440 ms). These results directly support the hypothesis that a significant subpopulation of NAc neurons inhibit palatable food consumption and that a pause in their firing is required to initiate and maintain consumption.

Symposium Overview

In rodents there is an important gustatory relay in the pontine parabrachial nucleus (PbN) upon which much centrifugal modulation occurs to guide complex feeding behaviors. From the PbN two separate projections arise, one which synapses in the parvicellular medial tip of the ventroposteromedial nucleus of the thalamus, which in turn sends axons to taste cortex. This pathway is thought to be largely sensory in nature. A second pathway projects widely to the ventral forebrain areas including hypothalamus, and amygdala and is thought to be largely affective in nature. Recent support for this dissociation comes from Hajnal and Norgren who found that lesions of the pons but not the thalamus disrupted dopamine overflow in the accumbens during sucrose licking. Remarkably, the pontine taste relay does not appear to exist in human and nonhuman primates, or if it does exist, its role is much reduced. The aim of this symposium is to outline the role of the PbN in sensory and affective processing of taste in rodents and to speculate upon the implications of interspecies differences for tasting and feeding in primates. The specific aim of the introductory comments will be to provide an overview of evidence for these interspecies differences to set the stage for the remaining papers.

Assessing the role of the growth hormone secretagogue receptor in motivational learning and food intake.

The orexigenic neuropeptide ghrelin is an endogeneous ligand for the growth hormone secretagogue receptor (GHS-R). This orexigen is expressed in both the periphery and in the central system, including portions of mesolimbic dopaminergic circuitry that play a role in affective behaviors. Here we examined pharmacological antagonism of GHS-R in motivational incentive learning, as reflected in Pavlovian-to-instrumental transfer (PIT). Furthermore, it is currently unclear whether the previous effects of ghrelin on food intake are mediated by pre- and/or postingestive influences on ingestive behavior. Thus, the authors also conducted detailed analyses of the temporal dynamics of sucrose licking. Mice received low (50 nmol), moderate (100 nmol), and high (200 nmol) intraperitoneal injections of the GHS-R antagonist GHRP-6 [D-Lys3] prior to subsequent transfer and sucrose consumption tests. Low and moderate doses led to an augmentation of PIT, while high dose injections led to generalized performance deficits. In addition, moderate and high doses of the antagonist resulted in reductions in sucrose intake by reducing palatability of the sucrose. These results suggest dissociable functions of GHS-R in its influence over motivational learning and ingestive behavior.

D-amphetamine enhances gustatory responses in brief access tests, but withdrawal does not produce gustatory anhedonia.

Withdrawal from chronic d -amphetamine (AMPH), a putative animal model of anhedonia and depression, has been shown to reduce reward function, including operant and consummatory responses for 4% sucrose. However, a using microstructural analysis of licking for 4% sucrose, we found that AMPH withdrawal failed to alter measures associated with gustatory evaluation. To further explore the anhedonia hypothesis, we evaluated licking for sucrose in brief access tests before, during, and following AMPH treatment. Rats received a series of either 12 escalating AMPH doses (1–10 mg/kg, i.p.; n =10) or isotonic saline ( n =6) injections over 4 days. Licking for an array of 7 sucrose solutions (in M, 0, 0.015, 0.031, 0.062, 0.125, 0.25, and 0.5), presented randomly 4 times daily (20 s trials), was recorded starting 2 days before the start of AMPH/saline administration and ending 5 days after AMPH/saline withdrawal. Both AMPH and saline groups expressed sigmoidal concentration-licking functions, with no between-group differences in licking on baseline days ( p 's >0.23). Relative to saline, 3 days of AMPH treatment increased licking for 0.015, 0.031, and 0.0625 M sucrose, producing a left-shift in the concentration-licking curve. No significant decline in sucrose licking was observed after AMPH withdrawal. These results suggest that AMPH enhanced gustatory evaluation, but that the processes mediating AMPH withdrawal-induced behavioral suppressions are unrelated to the hedonic evaluation of palatable taste stimuli.

Effects of melanin-concentrating hormone on licking microstructure and brief-access taste responses

The effects of intracerebroventricular application of melanin-concentrating hormone (MCH) on licking for sucrose, quinine hydrochloride (QHCl), and water solutions were evaluated in two experiments. In experiment 1, rats received 90-min access to sucrose and water solutions after MCH or vehicle microinjection to the third ventricle (3V). MCH increased intake largely through increases in the rate of licking early in the meal and in the mean duration of lick bursts, suggesting an effect on gustatory evaluation. Therefore, in experiment 2, brief access tests were used with a series of sucrose and QHCl concentrations to behaviorally isolate the effects of intracerebroventricular MCH on gustatory evaluation. MCH uniformly increased licking for all sucrose solutions, water, and weak concentrations of QHCl; however, it had no effect on licking for the strongest concentrations of QHCl, which were generally avoided under control conditions. Thus MCH did not produce nonspecific increases in oromotor activity, nor did it change the perceived intensity of the tastants. We conclude that MCH enhanced the gain of responses to normally accepted stimuli at a phase of processing after initial gustatory detection and after the decision to accept or reject the taste stimulus. A comparison of 3V NPY and MCH effects on licking microstructure indicated that these two peptides increased intake via dichotomous behavioral processes; although NPY suppressed measures associated with inhibitory feedback from the gut, MCH appeared instead to enhance measures associated with hedonic taste evaluation.

Taste pathways that mediate accumbens dopamine release by sapid sucrose

Although it has been associated with the release of dopamine in the forebrain, reward remains a conundrum in neuroscience. Sucrose is inherently rewarding and its sensory message reaches the brain via the gustatory system. In rodents, the central gustatory system bifurcates in the pontine parabrachial nuclei, one arm forming a standard thalamocortical axis, the other distributing widely in the limbic forebrain. We report here that lesions of the gustatory thalamus fail to affect dopamine overflow during sucrose licking (149±5% vs. 149±4% for controls). Similar damage to the parabrachial nuclei, which severs the limbic taste projection, substantially reduces dopamine release from the nucleus accumbens (121±4% vs. 168±9% for sham operated controls; p<0.02). This represents the first demonstration that the affective character of a sensory stimulus might separate from the thalamocortical system as early as the second central synapse.

Accumbens dopamine mechanisms in sucrose intake

Extracellular levels of dopamine (DA) and monoamine metabolites were measured in the nucleus accumbens (NAcc) during sucrose licking using microdialysis in freely moving rats. The converse relationship also was tested. Using bilateral reverse microdialysis, D1 and D2 receptor antagonists (SCH23390, sulpiride) and the DA uptake blocker nomifensine were introduced into NAcc while measuring both ingestive behavior and neurochemistry. Licking of 0.3 M sucrose caused a 305% (±69%) increase in NAcc DA compared with water intake. Reverse microdialysis of nomifensine at a dose that increased accumbens DA levels (1484±346%) led to an increase of sucrose intake (152.5±5.4%). Concurrent infusions of the D1 and D2 blockers with nomifensine brought sucrose ingestion back near to control levels (114.8±3.7%). The higher dose of the D2 antagonist sulpiride also increased DA levels and sucrose intake. In contrast, the lower dose of the D2, and both doses of the D1 antagonist had no chemical or behavioral effects. These results showed release of NAcc DA in response to sucrose licking and the converse, an augmentation of the behavior by uptake blockade. The same data, however, failed to prove that tonic, local accumbens D1 and D2 receptor activity influenced this ingestive behavior.

Insulin and raclopride combine to decrease short-term intake of sucrose solutions

We have previously reported that the hormone insulin can modulate synaptic function of dopamine neurons. To evaluate whether insulin can alter performance of a task which is dependent on intact dopaminergic signaling, we tested rats in a five minute lick rate task, with a range of concentrations of sucrose or oil solutions. Rats received either ip (t –15 min) saline or the D2 receptor antagonist raclopride (50 μg/kg), and intraventricular (t –4 h) saline or insulin (5 mU). Although ineffective on its own, insulin combined with raclopride treatment resulted in significant suppression of sucrose lick rates compared to the saline/saline group. The overall results are consistent with our hypothesis that insulin may modify performance in tasks that are dependent on dopaminergic signaling.

Ovariectomy and Estradiol Affect Postingestive Controls of Sucrose Licking

Hrupka, B. J., G. P. Smith and N. Geary. Ovariectomy and estradiol affect postingestive controls of sucrose licking. Physiol Behav 61(2) 243–247, 1997.—Ovariectomy (OVX) has been shown to increase, and estradiol replacement to decrease, meal size in rats. Because little is known about how estradiol influences meals, we conducted two experiments to examine the effects of OVX and β-estradiol 3-benzoate (EB) replacement on the microstructure of licking behavior. In both experiments, patterns of licking were analyzed in adult female Sprague–Dawley rats during an 0.8 M sucrose test meal. In Experiment 1, meal microstructure was determined preOVX and 10–12 days postOVX. Rate of licking following OVX was not changed during min 1 of the meal, but was significantly faster during min 2–4 of the meal (p < 0.03). The numbers of bursts (runs of licks separated by 250–500 ms) and numbers of clusters (runs of licks separated by > 500 ms) were significantly increased during min 2–4 (p < 0.05). In Experiment 2, OVX rats received EB replacement. Rate of licking after EB replacement was not changed during min 1 of the meal, but was significantly slower during the remainder of the meal (min 2–4, min 5–7, and min 8–10). Burst size, cluster size, and interburst interval were less after EB replacement during min 5–7 of the test meal (all p < 0.05). Because both OVX and EB replacement failed to alter the rate of licking during min 1, estrogen did not appear to alter the palatability of sucrose. OVX and EB replacement did appear to affect a postingestive mechanism(s) that is engaged within 2–4 min of meal onset.

Microstructural analysis of successive negative contrast in free-feeding and deprived rats

Rats shifted from 1.0 M to 0.1 M sucrose lick at lower rates for the weaker solution than rats that have continual access to the 0.1 M sucrose solution only. This effect, referred to as successive negative contrast, has been investigated primarily in food-deprived rats and, in all cases, using total licks or total volume consumed as the dependent measure. The present experiment used a microstructural analysis of licking patterns to examine the changes in behavior that constitute the contrast effect in total licks in both deprived and free-feeding rats. Although the magnitude of the effect was similar, deprived rats recovered from contrast more rapidly than free-feeding rats. Furthermore, the patterns of licking behavior associated with contrast differed under the two deprivation conditions. Specifically, when compared with the unshifted controls, the contrast effect in deprived rats was accomplished through a decrease in the number of licks per burst, an increase in the number of bursts initiated, a brief increase in the length of the interburst intervals, and no change in length of the interlick intervals. In free-feeding animals, contrast was associated with a decrease in the number of licks per burst, a brief increase in the length of the interburst interval, and no changes in either the number of bursts initiated or in the length of the interlick intervals. Together, these data demonstrate that patterns of licking behavior are differentially affected by solution concentration, deprivation state, and relative aspects of reward value.

D-Fenfluramine: Effects On Microstructure of Licking for Water and Sucrose

D-Fenfluramine: Effects On Microstructure of Licking for Water and Sucrose

Effect of taste context and ambient context changes on successive negative contrast

Rats shifted from 32% sucrose to 4% sucrose lick less than rats that experience oniy the 4% solution. Previous experiments have found this negative contrast effect to be reduced (“disinhibited”) by the addition of a novel tone in the postshift period. In Experiment 1 of this paper, the negative contrast effect was enhanced when a novel flavor was added to the sucrose solution in the postshift period. In Experiments 2–4, changes in the ambient context, even changes sufficient to produce disruptions in licking, did not alter the degree of negative contrast. Tiese results suggest that (1) rats compare rewards across substantially different contexts, (2) contrast may serve to enhance taste neophobia, and (3) a disinhibitory effect may be confined to the presentation of punctate, nontaste, novel stimuli within a familiar context.