Brainstem lesions and gustatory function: III. The role of the nucleus of the solitary tract and the parabrachial nucleus in retention of a conditioned taste aversion in rats.

1997 ◽  
Vol 111 (1) ◽  
pp. 180-187 ◽  
Author(s):  
Patricia S. Grigson ◽  
Tsuyoshi Shimura ◽  
Ralph Norgren
2002 ◽  
Vol 131 (1-2) ◽  
pp. 205-209 ◽  
Author(s):  
Matilde Lopez Grancha ◽  
Montserrat Navarro ◽  
Imaculada Cubero ◽  
Todd E Thiele ◽  
Ilene L Bernstein

2020 ◽  
Author(s):  
Paul V. Sabatini ◽  
Henriette Frikke-Schmidt ◽  
Joe Arthurs ◽  
Desiree Gordian ◽  
Anita Patel ◽  
...  

AbstractTo determine the function and mechanisms of action for hindbrain neurons that express GFRAL, the receptor for the anorexigenic peptide, GDF-15, we generated Gfralcre and conditional GfralCreERT mice. While signals of infection or pathophysiologic states (rather than meal ingestion) stimulate GFRAL neurons, the artificial activation of GfralCre- expressing neurons inhibited feeding, decreased gastric emptying, and promoted a conditioned taste aversion (CTA). Additionally, activation of the smaller population of GFRAL neurons captured by the GfralCreERT allele decreased gastric emptying and produced a CTA without suppressing food intake, suggesting that GFRAL neurons primarily modulate gastric physiology and stimulate aversive responses. GFRAL neurons most strongly innervated the parabrachial nucleus (PBN), where they targeted CGRP-expressing (CGRPPBN) neurons. Silencing CGRPPBN neurons abrogated the aversive and anorexic effects of GDF-15. These findings suggest that GFRAL neurons link non-meal-associated, pathophysiologic signals to the aversive suppression of nutrient uptake and absorption.


1989 ◽  
Vol 256 (2) ◽  
pp. R306-R312 ◽  
Author(s):  
G. L. Edwards ◽  
R. C. Ritter

Lesions of the area postrema and adjacent nucleus of the solitary tract (AP lesions) cause rats to consume increased amounts of palatable food in short duration tests. Because the lateral parabrachial nucleus (lPBN) receives a prominent afferent projection from the AP and adjacent nucleus of the solitary tract, it is possible the lPBN plays a role in the altered ingestive behaviors observed in AP-lesioned rats. The present study examines the role of the lPBN in overingestion of highly palatable foods subsequent to AP lesions. We found that lesions of the lPBN alone did not cause rats to consume increased amounts of palatable food. Rather, when lPBN lesions were produced before AP lesions, increased intake of highly palatable food did not occur. Moreover, when AP-lesioned rats received subsequent lPBN lesions, the previously established overingestion of palatable foods was abolished. These results indicate that the lPBN is necessary in the pathogenesis of AP lesion-induced overingestion of highly palatable foods.


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