Neural Mechanisms of Anorexia

Watts, Alan G.; Salter, Dawna

doi:10.1007/0-306-48643-1_14

Cited by 7 publications

(9 citation statements)

References 243 publications

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“…This notion would be consistent with our observations that all types of feeding so far examined are suppressed by DE, despite a diversity of stimuli that contribute to their expression (30,31,46,49,54).…”

Section: Perspectives and Significancesupporting

confidence: 90%

“…Furthermore, the fact that 2DG-stimulated feeding is normal after complete chemical ablation of mediobasal hypothalamic neurons that express NPY receptors (3) supports the notion that the inhibition of 2DG feeding by drinking hypertonic saline is not initiated at the level of the ARH. Rather, our more recent findings suggest that one reason DE animals remain anorexic is the significantly reduced sensitivity of some of their NPY target sites, particularly the PVH and LHA (30,49,54).…”

Section: Discussionmentioning

confidence: 79%

“…This particular part of the LHA was chosen because it included the perifornical area of the hypothalamus (see 40), as well as those parts that contain melaninstimulating hormone and orexin/hypocretin-producing neurons (43). These regions are strongly implicated in regulating feeding (32,37), as well as the development of DE-anorexia (16,49,52,55).…”

Section: Image Analysismentioning

confidence: 99%

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The role of hypothalamic ingestive behavior controllers in generating dehydration anorexia: a Fos mapping study

Salter‐Venzon¹,

Watts²

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Salter-Venzon D, Watts AG. The role of hypothalamic ingestive behavior controllers in generating dehydration anorexia: a Fos mapping study. Am J Physiol Regul Integr Comp Physiol 295: R1009 -R1019, 2008. First published July 30, 2008 doi:10.1152/ajpregu.90425.2008.-Giving rats 2.5% saline to drink for 3-5 days simply and reliably generates anorexia. Despite having the neurochemical and hormonal markers of negative energy balance, dehydrated anorexic rats show a marked suppression of spontaneous food intake, as well as the feeding that is usually stimulated by overnight starvation or a 2-deoxy-D-glucose (2DG) challenge. These observations are consistent with a dehydration-dependent inhibition of the core circuitry that controls feeding. We hypothesize that this inhibition is directed at those neurons in the paraventricular nucleus and lateral hypothalamic area that constitute the hypothalamic "behavior controller" for feeding rather than their afferent inputs from the arcuate nucleus or hindbrain that convey critical feeding-related sensory information. To test this hypothesis, we mapped and quantified the Fos-immunoreactive response to 2DG in control and dehydrated rats drinking 2.5% saline. Our rationale was that regions showing an attenuated Fos response to 2DG in dehydrated animals would be strong candidates as the targets of dehydration-induced suppression of 2DG feeding. We found that the Fos response to combined dehydration and 2DG was attenuated only in the lateral hypothalamic area, with dehydration alone increasing Fos in the lateral part of the paraventricular nucleus. In the arcuate nucleus and those regions of the hindbrain that provide afferent inputs critical for the feeding response to 2DG, the Fos response to 2DG was unaffected by dehydration. Therefore, dehydration appears to target the lateral hypothalamic area and possibly the lateral part of the paraventricular nucleus to suppress the feeding response to 2DG. feeding behavior; inhibition; 2-deoxyglucose; arcuate nucleus; hindbrain; parabrachial nucleus; area postrema; nucleus of the solitary tract ANOREXIA IS A LOSS OF APPETITE in the presence of adequate food sources and can be physiologically or pathologically generated (49). We have previously shown that animals develop anorexia after drinking hypertonic saline and becoming dehydrated (DE). These animals provide a useful model for investigating the underlying neural mechanisms of anorexia (47-49, 54).DE-anorexic rats limit their spontaneous circadian-driven food intake despite the presence of endocrine and neuropeptidergic profiles of negative energy balance (55). In fact, DE animals share a virtually identical profile of caloric deficit markers with animals that are food restricted to match the intake of their anorexic counterparts (55). This profile includes body weight loss, undetectable levels of circulating leptin and insulin, increased plasma glucocorticoid concentrations, and elevated neuropeptide Y (NPY) gene expression in the arcuate nucleus of the hypothalamus (ARH). While these...

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Section: Perspectives and Significancesupporting

confidence: 90%

Section: Discussionmentioning

confidence: 79%

Section: Image Analysismentioning

confidence: 99%

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The role of hypothalamic ingestive behavior controllers in generating dehydration anorexia: a Fos mapping study

Salter‐Venzon¹,

Watts²

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The 30 minute feeding response to 50ng of muscimol injected bilaterally into the shell of the nucleus accumbens of dehydrated by drinking 2.5% hypertonic saline is inversely correlated to the intensity of the resulting anorexia (Data adapted from [36]). A) Ingestive behavior control is thought to be controlled by a brain-wide network that converges onto a motor control network, which is organized at three levels [adapted from 10,11,12,18]: A hypothalamic behavior controller that contains drive circuits that can either stimulate, or inhibit behaviors; action selection networks that integrate the outputs of the hypothalamic controller with those of other systems; and executive pre-motor and motor neuron networks. The generation of motivated behavioral actions by motor control networks can be initiated by a variety of inputs.…”

Section: Discussionmentioning

confidence: 99%

“…As yet unidentified elements in the PVH appear to contribute to the behavioral controller for feeding. A great deal of structural and experimental evidence also strongly implicates parts of the LHA as being important contributors to the control network [see 18 for review]. The overall control functions of the PVH and parts of the LHA on ingestive behaviors are then mediated by their connections to the hindbrain and telencephalon (Fig.…”

Section: Network Convergencementioning

confidence: 99%

Neural network interactions and ingestive behavior control during anorexia

Watts

Salter

Neuner

2007

Physiology & Behavior

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Many models have been proposed over the years to explain how motivated feeding behavior is controlled. One of the most compelling is based on the original concepts of Eliot Stellar whereby sets of interosensory and exterosensory inputs converge on a hypothalamic control network that can either stimulate or inhibit feeding. These inputs arise from information originating in the blood, the viscera, and the telencephalon. In this manner the relative strengths of the hypothalamic stimulatory and inhibitory networks at a particular time dictates how an animal feeds. Anorexia occurs when the balance within the networks consistently favors the restraint of feeding. This article discusses experimental evidence supporting a model whereby the increases in plasma osmolality that result from drinking hypertonic saline activate pathways projecting to neurons in the paraventricular nucleus of the hypothalamus (PVH) and lateral hypothalamic area (LHA). These neurons constitute the hypothalamic controller for ingestive behavior, and receive a set of afferent inputs from regions of the brain that process sensory information that is critical for different aspects of feeding. Important sets of inputs arise in the arcuate nucleus, the hindbrain, and in the telencephalon. Anorexia is generated in dehydrated animals by way of osmosensitive projections to the behavior control neurons in the PVH and LHA, rather than by actions on their afferent inputs.

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Rapid and preferential activation of Fos protein in hypocretin/orexin neurons following the reversal of dehydration‐anorexia

Watts

Sanchez‐Watts

2007

J of Comparative Neurology

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Dehydration (DE)-anorexia is stimulated by chronic consumption of hypertonic saline. Spontaneous nocturnal food intake is markedly reduced with this treatment but is rapidly reversed upon the return of drinking water. Here we examined the neurons in the lateral hypothalamic area (LHA) of chronically dehydrated rats for their peptidergic phenotype, colocalization, and activation profiles following the rapid reversal of anorexia. To do this, we used double-labeling combinations of Fos immunocytochemistry and radioisotopic- and digoxigenin-labeled in situ hybridization. We found that lateral hypothalamic corticotropin-releasing hormone (CRH) neurons show extensive coexpression with neurotensin mRNA, but they are distinct from hypocretin/orexin and melanin-concentrating hormone (MCH) neurons. Chronic dehydration increases Fos-ir in large numbers of neurons in dorsal regions of the LHA. Some of these LHA neurons also show increased CRH, but not hypocretin/orexin or MCH gene expression, as dehydration-anorexia develops. Furthermore, the behavioral sequence of eating and increased activity exhibited by DE animals in the minutes following water drinking is accompanied by a further increase in the number of Fos-ir nuclei in the LHA. Increased Fos activation occurs in a significant number of LHA hypocretin/orexin neurons, but not CRH or MCH neurons, in the LHA. Together these data implicate CRH but not hypocretin/orexin or MCH neurons in the LHA in the motor events associated with dehydration. However, when water is returned, contributions to the network controlling responses evidently come from hypocretin/orexin, but not CRH or MCH, neurons in the LHA.

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Neural Mechanisms of Anorexia

Cited by 7 publications

References 243 publications

The role of hypothalamic ingestive behavior controllers in generating dehydration anorexia: a Fos mapping study

The role of hypothalamic ingestive behavior controllers in generating dehydration anorexia: a Fos mapping study

Neural network interactions and ingestive behavior control during anorexia

Rapid and preferential activation of Fos protein in hypocretin/orexin neurons following the reversal of dehydration‐anorexia

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