Gustatory functions, sodium appetite, and conditioned taste aversion survive excitotoxic lesions of the thalamic taste area.

Scalera, Giuseppe; Grigson, Patricia S.; Norgren, Ralph

doi:10.1037/0735-7044.111.3.633

Cited by 77 publications

(75 citation statements)

References 50 publications

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“…The suppressive effects of cocaine and sucrose, but not LiCl, are augmented in rats with a history of chronic morphine treatment [57]. Finally, bilateral lesions of the gustatory thalamus or gustatory cortex disrupt the suppressive effects of morphine, cocaine, and sucrose, but have no impact on the development of a LiCl-induced CTA [58][59][60][61][62][63][64][65]. Taken together, the data confirm that drug-induced suppression of CS intake is not mediated by a conditioned taste aversion like that induced by the aversive agent.…”

Section: The Model: Experimenter Delivered Drugmentioning

confidence: 99%

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Reward comparison: the Achilles’ heel and hope for addiction

Grigson

2008

Drug Discovery Today: Disease Models

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In the words of the late Charles Flaherty, reward comparison is commonplace. Rats and man, it appears, compare all rewards and this capacity likely contributes to our ability to select the most appropriate reward/behavior (food, water, salt, sex), at the most ideal level (e.g., a certain sweetness), at any given time. A second advantage of our predisposition for reward comparison is that the availability of rich alternative rewards can protect against our becoming addicted to any single reward/behavior. Thus, the potential protective effects of natural rewards/enrichment are addressed. Despite this, behavior can become inflexible when, through the development of addiction, stress, drug, or cues elicit craving, withdrawal, and ultimately, drug-seeking. Drug-seeking corresponds with a 'window of inopportunity', when even potent natural rewards have little or no impact on behavior. During this time, there is a unitary solution to the need state, and that solution is drug. The present animal model explores this 'window of inopportunity' when natural rewards are devalued and drug-seeking is engaged and considers a mode of possible intervention.

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Section: The Model: Experimenter Delivered Drugmentioning

confidence: 99%

“…They seek to satisfy this need state much as they seek food when hungry, water when thirsty, and salt when sodium deficient [65]. When these biological drive states are activated, there is a single goal and there can be no substitute.…”

Section: Competing Motivations: Closing the 'Window Of Inopportunity'mentioning

confidence: 99%

Reward comparison: the Achilles’ heel and hope for addiction

Grigson

2008

Drug Discovery Today: Disease Models

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“…For example, whereas the afferent projections from the PbN to the VPMpc were well documented, the efferent projections from the VPMpc to the PbN were not demonstrated (4,21,64). In addition, while earlier studies have shown that the VPMpc is involved in taste detection and discrimination (32), sodium appetite (30,44), and CTA (37,92,93), more recent studies have demonstrated that the VPMpc has a minimal influence on innate taste preference (15,62,78), sodium appetite (14,65), or CTA (14,65). Thorough reviews of earlier studies suggested that the claim of the involvement of VPMpc in taste preference, sodium appetite, and CTA were derived from the lesions that were misplaced, inordinately large, or destroyed fibers of passage (58,60,69).…”

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confidence: 94%

Modulation of activity of gustatory neurons in the hamster parabrachial nuclei by electrical stimulation of the ventroposteromedial nucleus of the thalamus

Mao¹,

Cho²,

Li³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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(VPMpc) is positioned at the key site between the gustatory parabrachial nuclei (PbN) and the gustatory cortex for relaying and processing gustatory information via the thalamocortical pathway. Although neuroanatomical and electrophysiological studies have provided information regarding the gustatory projection from PbN to VPMpc, the exact relationship between PbN and VPMpc, especially the efferent projection involving VPMpc to PbN, is obscure. Here we investigated the reciprocal connection between these two gustatory relays in urethaneanesthetized hamsters. We recorded from 114 taste-responsive neurons in the PbN and examined their responsiveness to electrical stimulation of the VPMpc bilaterally. Stimulation of either or both of the ipsilateral or contralateral VPMpc antidromically activated 109 gustatory PbN neurons. Seventy-two PbN neurons were antidromically activated after stimulation of both sides of the VPMpc, indicating that taste neurons in the PbN project heavily to the bilateral VPMpc. Stimulation of VPMpc also orthodromically activated 110 of PbN neurons, including 106 VPMpc projection neurons. Seventyeight neurons were orthodromically activated bilaterally. Among orthodromic activations of the PbN cells, the inhibitory response was the dominant response; 106 cells were inhibited, including 10 neurons that were also excited contralaterally, indicating that taste neurons in the PbN are subject to strong inhibitory control from VPMpc. Moreover, stimulation of VPMpc altered taste responses of the neurons in the PbN, indicating that VPMpc modulates taste responses of PbN neurons. These results may provide functional insight of neural circuitry for taste processing and modulation involving these two nuclei.central gustatory pathway; pons; electrophysiology THE PARABRACHIAL NUCLEI (PbN) and the parvicellular part of the ventroposteromedial nucleus of the thalamus (VPMpc) are the second and tertiary central relays for taste information processing in rodents, respectively (4,13,17,28,45,49,51). Gustatory information elicited from the tongue and oropharyngeal cavity is initially carried to the rostral portion of the nucleus of the solitary tract (NST) by the VIIth, IXth, and Xth cranial nerves, and these terminals are distributed in a topographic fashion with rostral-caudal sequence in the rostral NST (2,9,23,24,89). From the NST, ascending gustatory fibers project to third-order taste cells within the PbN of the pons (7,22,42,46,(53)(54)(55)87). Two separate routes carry taste information from the PbN further to the forebrain taste areas and cortex: the ventral forebrain pathway that involves the central nucleus of the amygdala (CeA), the lateral hypothalamus (LH), the bed nucleus of the stria terminalis (BNST), the substantia innominata (3,12,16,21,31,33,34,41,47,63,64,71); and the thalamocortical pathway that is characterized by the involvement of the bilateral VPMpc, which, in turn, carries taste information to the gustatory cortex (GC) (5,25,45,48,51).The PbN is a critical neural substrate for a number...

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“…Some studies have reported that VPMpc-lesioned animals retain a normal concentration response to preferred and non-preferred tastes [134][135][136][137] but may have disrupted [137], impaired [127,130] or else have no effects on CTA [134,135,138,139]. Current views suggest a role in comparing novel and familiar tastes [140] in more complex gustatory learning tasks or in attention to gustatory function [135,136,141].…”

Section: The Gustatory System In the Ratmentioning

confidence: 99%