Central gustatory lesions and learned taste aversions: Unconditioned stimuli

Mungarndee, Suriyaphun S.; Lundy, Robert F.; Norgren, Ralph

doi:10.1016/j.physbeh.2005.12.008

Cited by 23 publications

(20 citation statements)

References 35 publications

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“…For example, a number of reports show that lateral PBN lesions prevent the acquisition of CTAs (Mungarndee, Lundy, & Norgren, 2006;Navarro & Cubero, 2003;Reilly & Trifunovic, 2000aTrifunovic & Reilly, 2002). Similarly, lateral PBN lesions using ibotenic acid prevent the acquisition of caloriebased conditioned flavor preferences (Reilly & Trifunovic, 2000a) and disrupt the concentration-dependent intake of sucrose (Reilly & Trifunovic, 2000b).…”

Section: Discussionmentioning

confidence: 99%

C-fos expression in the rat brain following lithium chloride-induced illness

2007

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The present study examined c-Fos expression in selected brain areas consequent to administration of lithium chloride, the typical illness-inducing agent used in laboratory studies of conditioned taste aversion. The results replicated previous findings of significant c-Fos expression in the parabrachial nucleus, the central nucleus of the amygdala and the basolateral amygdala. New findings indicate significant lithium-induced c-Fos in the gustatory region of the thalamus and the bed nucleus of the stria terminalis but not in the insular cortex. The results are discussed with respect to the neural substrates of conditioned taste aversion.

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Section: Discussionmentioning

confidence: 99%

C-fos expression in the rat brain following lithium chloride-induced illness

2007

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“…Because the PBN/KF complex is a relay through which visceral signals reach higher centers of the brain, this region is believed to be critical in generating affective responses and sensations, such as nausea following interoceptive stimuli (4). Evidence that PBN/KF neurons are part of the nausea-generating pathway includes observations that these neurons express the intermediate-early gene c-fos during emetic stimuli (15) and that lesions of this area affect behaviors in rodents that are believed to indicate the presence of malaise, including pica responses (29) and acquisition of conditioned taste aversions (44,48,50,51,57,58).…”

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confidence: 99%

Integrative responses of neurons in parabrachial nuclei to a nauseogenic gastrointestinal stimulus and vestibular stimulation in vertical planes

Suzuki¹,

Sugiyama²,

Yates

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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In addition, the PBN/KF region receives inputs from the vestibular system and likely mediates the malaise associated with motion sickness. However, previous studies have not considered whether GI and vestibular inputs converge on the same PBN/KF neurons, and if so, whether the GI signals alter the responses of the cells to body motion. The present study, conducted in decerebrate cats, tested the hypothesis that intragastric injection of copper sulfate, which elicits emesis by irritating the stomach lining, modifies the sensitivity of PBN/KF neurons to vertical plane rotations that activate vestibular receptors. Intragastric copper sulfate produced a 70% median change in the gain of responses to vertical plane rotations of PBN/KF units, whose firing rate was modified by the administration of the compound; the response gains for 16 units increased and those for 17 units decreased. The effects were often dramatic: out of 51 neurons tested, 13 responded to the rotations only after copper sulfate was injected, whereas 10 others responded only before drug delivery. These data show that a subset of PBN/KF neurons, whose activity is altered by a nauseogenic stimulus also respond to body motion and that irritation of the stomach lining can either cause an amplification or reduction in the sensitivity of the units to vestibular inputs. The findings imply that nausea and affective responses to vestibular stimuli may be modified by the presence of emetic signals from the GI system.

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“…4 in Ref. 37 for both mPBNx and lPBNx groups; CS and water intakes are almost double that of controls); the normal feeding behavior of the same rats does not vary significantly from controls. The lPBN contains neurons that respond to gastric stretch, and it is possible that destruction of these cells removed this inhibitory pathway (4,5).…”

Section: Discussionmentioning

confidence: 76%

Chemotherapy-induced kaolin intake is increased by lesion of the lateral parabrachial nucleus of the rat

Horn

Jonghe

Mátyás

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Horn CC, De Jonghe BC, Matyas K, Norgren R. Chemotherapy-induced kaolin intake is increased by lesion of the lateral parabrachial nucleus of the rat. Am J Physiol Regul Integr Comp Physiol 297: R1375-R1382, 2009. First published August 26, 2009 doi:10.1152/ajpregu.00284.2009.-Anticancer agents, such as cisplatin, stimulate nausea, vomiting, and behaviors indicative of malaise. Rats and mice do not possess a vomiting response, and, therefore, in these species, the ingestion of kaolin clay (a pica response) has been used as an index of malaise. In the rat, cisplatininduced kaolin intake is inhibited by antiemetic treatments. In addition, cisplatin activates vagal afferent fibers in the gut, and kaolin intake induced by cisplatin is largely dependent on an intact vagus. Nevertheless, little is known about the brain pathways controlling pica. We investigated the role of the lateral parabrachial nucleus (lPBN), a major visceral afferent link between the hindbrain and forebrain, in cisplatin-induced c-Fos expression and pica. Injection of cisplatin (6 mg/kg ip) produced c-Fos expression in the ventrolateral (external) lPBN, a region receiving viscerosensory input. In rats with bilateral ibotenic acid lPBN lesions, cisplatin treatment substantially increased kaolin intake compared with controls (ϳ30 g vs. ϳ5 g, respectively, over 24 h). Food intake was reduced by cisplatin treatment and by apomorphine, an emetic agent that acts centrally. Unlike cisplatin, however, apomorphine stimulated kaolin intake to a similar degree in both the lesioned and control rats, suggesting that lPBN damage neither produces nonspecific effects nor enhances malaise in general. These data suggest that lPBN-lesioned animals not only demonstrate pica after cisplatin treatment, but, in fact, show an exaggerated response that is greatly in excess of any treatment known to produce kaolin intake in rats.emesis; nausea; pica; vagus; anorexia CANCER CHEMOTHERAPY AGENTS, such as cisplatin, stimulate nausea, vomiting, anorexia, and other behaviors indicative of malaise (for a review, see Refs. 2, 21, 27, 51). Several species, including dogs, cats, ferrets, pigs, and shrews, have been used to study emesis after treatment with chemotherapy agents (16,18,31,33,58). In contrast, laboratory rats and mice appear to lack a vomiting response (see Ref. 2 for review). For these species, kaolin intake has been used as a proxy for emesis (60,64). A wide variety of stimuli, including cisplatin, induce kaolin consumption in rats (36,53,59,60,65). Like emesis, geophagia appears to be a defensive response. Clay may serve to bind or dilute a toxin in the gastrointestinal (GI) tract, thus reducing its adverse effects (45, 46). After injection with cisplatin, rats consuming kaolin show less body weight loss and a smaller reduction in food intake than rats without kaolin access (12). The consumption of clay by humans is also recognized as a potential detoxification strategy (48).Despite the use of kaolin intake as an index of malaise in rats, very little is known about...

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Central gustatory lesions and learned taste aversions: Unconditioned stimuli

Cited by 23 publications

References 35 publications

C-fos expression in the rat brain following lithium chloride-induced illness

C-fos expression in the rat brain following lithium chloride-induced illness

Integrative responses of neurons in parabrachial nuclei to a nauseogenic gastrointestinal stimulus and vestibular stimulation in vertical planes

Chemotherapy-induced kaolin intake is increased by lesion of the lateral parabrachial nucleus of the rat

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