Excitotoxic lesions of the parabrachial nuclei prevent conditioned taste aversions and sodium appetite in rats.

Scalera, Giuseppe; Spector, Alan C.; Norgren, Ralph

doi:10.1037/0735-7044.109.5.997

Cited by 86 publications

(98 citation statements)

References 35 publications

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“…Such responses are indicative of altered sensory coding of salt taste and this information is conveyed to the second central gustatory relay center, the pontine parabrachial nucleus (PBN). Bilateral lesion of the PBN eliminates salt appetite stimulated by a variety of methods (Hill & Almli 1983, Flynn et al 1991, Spector et al 1993, Scalera et al 1995. However, it is the connections distal to the PBN that are believed to be critical for the expression of salt appetite because decerebrate rats, which have an intact PBN but severed connections to the forebrain, do not express a salt appetite (Grill et al 1986).…”

Section: Central Gustatory Processingmentioning

confidence: 99%

Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

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Nearly three-quarters of a century ago, Curt Richter removed the adrenal glands from rats and noted that the animal's vitality was dependent on its increased consumption of sodium chloride. In doing so, Richter revealed an innate behavioral mechanism that serves to maintain the hydromineral balance of an animal faced with sodium deficit. This experiment and others like it, led to the development of a field of research devoted to the investigation of salt appetite. The following is a discussion of how Richter's initial observations gave birth to an evolving field that incorporates multiple approaches to examine the drive to consume sodium. KeywordsSalt appetite; Angiotensin; Aldosterone; Corticosterone; Richter The Discovery of Salt AppetiteAt the time that Richter began his career at Johns Hopkins University much of the research examining ingestive behavior focused on the responses of individual organs or closely coordinated systems. Richter's pioneering work initiated a fundamental paradigm shift that moved the focus to adaptations of the organism as a whole. Specifically, he was interested in changes in behavior that compensated for perturbations in the internal environment. His approach toward investigation of such behaviors was as thorough as it was fundamental. Richter manipulated diet, interfered with the nervous system, and removed or replaced glandular secretions in attempt to understand the nutritional, neural, and endocrine signals that contribute to behavior.Richter created disturbances in the nutritional or mineral content of the internal environment with dietary deficiency. Subsequently, "self selection" experiments were performed where choices of different minerals and nutrients were presented for consumption. More often than not, animals would consume minerals and nutrients in amounts that would alleviate their experimentally-induced deficiencies. One of the most striking behaviors that Richter observed was that of rats voluntarily ingesting salt when faced with sodium deficit. Sodium chloride was removed from the rats' food and they were given access to water and 3 % NaCl solution. The intake of the NaCl solution was approximately 1% of the total diet, which remarkably, is the

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Section: Central Gustatory Processingmentioning

confidence: 99%

Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

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“…Our neural tracing studies have revealed that the HSD2 neurons primarily innervate rostral brain sites that previously have been implicated in sodium appetite (our unpublished observations), including subnuclei within the pontine parabrachial region (Scalera et al, 1995) and the bed nucleus of the stria terminalis (Reilly et al, 1994;Zardetto-Smith et al, 1994). It also should be noted that small NTS lesions, lateral to the HSD2 neurons and area postrema, eliminate baroreflex regulation of blood pressure and heart rate yet leave sodium appetite intact (Schreihofer et al, 1999).…”

Section: Hsd2 Neurons As a Neuroanatomical Link To Sodium Appetitementioning

confidence: 99%

Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

Geerling¹,

Engeland²,

Kawata³

et al. 2006

J. Neurosci.

132

187

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Sodium appetite can be enhanced by the adrenal steroid aldosterone via an unknown brain mechanism. A novel group of neurons in the nucleus tractus solitarius expresses the enzyme 11-␤-hydroxysteroid dehydrogenase type 2, which makes them selectively responsive to aldosterone. Their activation parallels sodium appetite in different paradigms of salt loss even in the absence of aldosterone. These unique aldosterone target neurons may represent a previously unrecognized central convergence point at which hormonal and neural signals can be integrated to drive sodium appetite.

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“…Gustatory responses of PbN neurons to NaCl in sodium-deprived rats were reduced relative to the control animals (70). Lesions of PbN also block the expression of a sodium appetite in rats (14,66), suggesting that PbN is involved in mediating sodium appetite.In addition, studies have demonstrated that lesions of the PbN prevent acquisition of CTA in rats (19,59,69,77,90).A number of anatomical and electrophysiological studies have shown strong neuronal connections between the PbN and forebrain gustatory nuclei. The efferent projections to the gustatory PbN from the LH, CeA, BNST, and GC were demonstrated in rats and hamsters (41,83,84,88,94).…”

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confidence: 99%

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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Excitotoxic lesions of the parabrachial nuclei prevent conditioned taste aversions and sodium appetite in rats.

Cited by 86 publications

References 35 publications

Richter and sodium appetite: From adrenalectomy to molecular biology

Richter and sodium appetite: From adrenalectomy to molecular biology

Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

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

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