Trends in the functional morphology and sensorimotor control of feeding behavior in salamanders: An example of the role of internal dynamics in evolution

1985 ◽  
Vol 34 (2-4) ◽  
pp. 175-191 ◽  
Author(s):  
Gerhard Roth ◽  
David B. Wake
Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4356-4367 ◽  
Author(s):  
Jennifer E. Richard ◽  
Imre Farkas ◽  
Fredrik Anesten ◽  
Rozita H. Anderberg ◽  
Suzanne L. Dickson ◽  
...  

Abstract The parabrachial nucleus (PBN) is a key nucleus for the regulation of feeding behavior. Inhibitory inputs from the hypothalamus to the PBN play a crucial role in the normal maintenance of feeding behavior, because their loss leads to starvation. Viscerosensory stimuli result in neuronal activation of the PBN. However, the origin and neurochemical identity of the excitatory neuronal input to the PBN remain largely unexplored. Here, we hypothesize that hindbrain glucagon-like peptide 1 (GLP-1) neurons provide excitatory inputs to the PBN, activation of which may lead to a reduction in feeding behavior. Our data, obtained from mice expressing the yellow fluorescent protein in GLP-1-producing neurons, revealed that hindbrain GLP-1-producing neurons project to the lateral PBN (lPBN). Stimulation of lPBN GLP-1 receptors (GLP-1Rs) reduced the intake of chow and palatable food and decreased body weight in rats. It also activated lPBN neurons, reflected by an increase in the number of c-Fos-positive cells in this region. Further support for an excitatory role of GLP-1 in the PBN is provided by electrophysiological studies showing a remarkable increase in firing of lPBN neurons after Exendin-4 application. We show that within the PBN, GLP-1R activation increased gene expression of 2 energy balance regulating peptides, calcitonin gene-related peptide (CGRP) and IL-6. Moreover, nearly 70% of the lPBN GLP-1 fibers innervated lPBN CGRP neurons. Direct intra-lPBN CGRP application resulted in anorexia. Collectively, our molecular, anatomical, electrophysiological, pharmacological, and behavioral data provide evidence for a functional role of the GLP-1R for feeding control in the PBN.


Author(s):  
Brian Hayden

The Akha constitute the relatively poor end of the hill tribe spectrum, but they have a wide range of feasts that employ the available surplus production. This chapter shows how Akha feasts support the economic, ritual, and sociopolitical organization of communities. The role of taboos as aggrandizer strategies is explored and the internal dynamics of the ritual-political structure of villages is examined. Examples of the range of Akha feasts are described and explanations provided in terms of how they dovetail with various levels of sociopolitical groups, including household, clan, administrative, and village levels, but especially lineages. The important issue of why some households do not participate in feasts is raised. Material patterning of feasts is again discussed.


2008 ◽  
Vol 68 (1) ◽  
pp. 221-228 ◽  
Author(s):  
F. Abrunhosa ◽  
M. Melo

The development of the foregut structure and the digestive function of the decapods Litopenaeus vannamei, Sesarma rectum and Callichirus major larvae and post larvae were examined. The protozoeal foregut of L. vannamei is simple, lacking a cardiopyloric valve and bearing a rudimentary filter press. In mysis, the filter press is more developed. In the juvenile stage, grooves and a small lateral tooth arise. In S. rectum, the foregut has a functional cardiopyloric valve and a filter press. The megalopal and juvenile stages of this species have a gastric mill similar to those in adult crabs. In C. major, the foregut of the zoeae is specialized, with the appearance of some rigid structures, but no gastric mill was found. Calcified structures are observed in the megalopae and they become more developed in the juvenile stage. The results support suppositions, previously reported in other studies, that feeding behavior of each larval and postlarval stage is directly related to the morphological characteristics of the foreguts.


2009 ◽  
Vol 296 (3) ◽  
pp. R587-R594 ◽  
Author(s):  
Premysl Bercik ◽  
Elena F. Verdú ◽  
Jane A. Foster ◽  
Jun Lu ◽  
Angela Scharringa ◽  
...  

Bacterial infection can trigger the development of functional GI disease. Here, we investigate the role of the gut-brain axis in gastric dysfunction during and after chronic H. pylori infection. Control and chronically H. pylori-infected Balb/c mice were studied before and 2 mo after bacterial eradication. Gastric motility and emptying were investigated using videofluoroscopy image analysis. Gastric mechanical viscerosensitivity was assessed by cardioautonomic responses to distension. Feeding patterns were recorded by a computer-assisted system. Plasma leptin, ghrelin, and CCK levels were measured using ELISA. IL-1β, TNF-α, proopiomelanocortin (POMC), and neuropeptide Y mRNAs were assessed by in situ hybridizations on frozen brain sections. Gastric inflammation was assessed by histology and immunohistochemistry. As shown previously, H. pylori-infected mice ate more frequently than controls but consumed less food per bout, maintaining normal body weight. Abnormal feeding behavior was accompanied by elevated plasma ghrelin and postprandial CCK, higher TNF-α (median eminence), and lower POMC (arcuate nucleus) mRNA. Infected mice displayed delayed gastric emptying and visceral hypersensitivity. Eradication therapy normalized gastric emptying and improved gastric sensitivity but had no effect on eating behavior. This was accompanied by persistently increased TNF-α in the brain and gastric CD3+ T-cell counts. In conclusion, chronic H. pylori infection in mice alters gastric emptying and mechanosensitivity, which improve after bacterial eradication. A feeding pattern reminiscent of early satiety persists after H. pylori eradication and is accompanied by increased TNF-α in the brain. The results support a role for altered gut-brain pathways in the maintenance of postinfective gut dysfunction.


2011 ◽  
Vol 105 (2) ◽  
pp. 846-859 ◽  
Author(s):  
Lore Thaler ◽  
Melvyn A. Goodale

Studies that have investigated how sensory feedback about the moving hand is used to control hand movements have relied on paradigms such as pointing or reaching that require subjects to acquire target locations. In the context of these target-directed tasks, it has been found repeatedly that the human sensory-motor system relies heavily on visual feedback to control the ongoing movement. This finding has been formalized within the framework of statistical optimality according to which different sources of sensory feedback are combined such as to minimize variance in sensory information during movement control. Importantly, however, many hand movements that people perform every day are not target-directed, but based on allocentric (object-centered) visual information. Examples of allocentric movements are gesture imitation, drawing, or copying. Here we tested if visual feedback about the moving hand is used in the same way to control target-directed and allocentric hand movements. The results show that visual feedback is used significantly more to reduce movement scatter in the target-directed as compared with the allocentric movement task. Furthermore, we found that differences in the use of visual feedback between target-directed and allocentric hand movements cannot be explained based on differences in uncertainty about the movement goal. We conclude that the role played by visual feedback for movement control is fundamentally different for target-directed and allocentric movements. The results suggest that current computational and neural models of sensorimotor control that are based entirely on data derived from target-directed paradigms have to be modified to accommodate performance in the allocentric tasks used in our experiments. As a consequence, the results cast doubt on the idea that models of sensorimotor control developed exclusively from data obtained in target-directed paradigms are also valid in the context of allocentric tasks, such as drawing, copying, or imitative gesturing, that characterize much of human behavior.


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