scholarly journals The functional link between tail-pinch-induced food intake and emotionality and its possible role in stress coping in rats

2018 ◽  
Vol 68 (6) ◽  
pp. 799-805 ◽  
Author(s):  
Nami Aso-Someya ◽  
Kimiya Narikiyo ◽  
Akira Masuda ◽  
Shuji Aou
2019 ◽  
Vol 38 (3) ◽  
pp. 238-247 ◽  
Author(s):  
Tyler B. Mason ◽  
Sydney G. O'Connor ◽  
Susan M. Schembre ◽  
Jimi Huh ◽  
Daniel Chu ◽  
...  
Keyword(s):  

2011 ◽  
Vol 71 ◽  
pp. e165-e166
Author(s):  
Nami Someya ◽  
Kimiya Narikiyo ◽  
Akira Masuda ◽  
Shuji Aou
Keyword(s):  

Neuroscience ◽  
2003 ◽  
Vol 116 (2) ◽  
pp. 519-524 ◽  
Author(s):  
S. Samarghandian ◽  
H. Ohata ◽  
N. Yamauchi ◽  
T. Shibasaki

2014 ◽  
Vol 306 (3) ◽  
pp. R164-R174 ◽  
Author(s):  
Miriam Goebel-Stengel ◽  
Andreas Stengel ◽  
Lixin Wang ◽  
Yvette Taché

Tail pinch stimulates food intake in rats. We investigated brain mechanisms of this response and the influence of repeated exposure. Sprague-Dawley rats received acute (5 min) or repeated (5 min/day for 14 days) tail pinch using a padded clip. Acute tail pinch increased 5-min food intake compared with control (0.92 ± 0.2 vs. 0.03 ± 0.01 g, P < 0.01). This response was inhibited by 76% by intracerebroventricular injection of BIBP-3226, a neuropeptide Y1 (NPY1) receptor antagonist, increased by 48% by astressin-B, a corticotropin-releasing factor (CRF) receptor antagonist, and not modified by S-406-028, a somatostatin subtype 2 antagonist. After the 5-min tail pinch without food, blood glucose rose by 21% ( P < 0.01) while changes in plasma acyl ghrelin (+41%) and adrenocorticotropic hormone (+37%) were not significant. Two tail pinches (45 min apart) activate pontine and hindbrain catecholaminergic and hypothalamic paraventricular CRF neurons. After 14 days of repeated tail pinch, the 5-min orexigenic response was not significantly different from days 2 to 11 but reduced by 50% thereafter ( P < 0.001). Simultaneously, the 5-min fecal pellet output increased during the last 5 days compared with the first 5 days (+58%, P < 0.05). At day 14, the body weight gain was reduced by 22%, with a 99% inhibition of fat gain and a 25% reduction in lean mass ( P < 0.05). The orexigenic response to acute 5-min tail pinch is likely to involve the activation of brain NPY1 signaling, whereas that of CRF tends to dampen the acute response and may contribute to increased defecation and decreased body weight gain induced by repeated tail pinch.


Appetite ◽  
2010 ◽  
Vol 54 (3) ◽  
pp. 669
Author(s):  
A.K. Portella ◽  
V. Bittencourt ◽  
S. Cardoso ◽  
C. Dalmaz ◽  
P.P. Silveira ◽  
...  

Life Sciences ◽  
1984 ◽  
Vol 35 (2) ◽  
pp. 163-170 ◽  
Author(s):  
Gyula Telegdy ◽  
Tibor Kádár ◽  
Kálmán Kovács ◽  
Botond Penke
Keyword(s):  

2016 ◽  
Vol 28 (5) ◽  
Author(s):  
M. H. Hu ◽  
Z. Bashir ◽  
X. F. Li ◽  
K. T. O'Byrne

2019 ◽  
Vol 476 (21) ◽  
pp. 3281-3293 ◽  
Author(s):  
Elodie Lebredonchel ◽  
Marine Houdou ◽  
Hans-Heinrich Hoffmann ◽  
Kateryna Kondratska ◽  
Marie-Ange Krzewinski ◽  
...  

TMEM165 was highlighted in 2012 as the first member of the Uncharacterized Protein Family 0016 (UPF0016) related to human glycosylation diseases. Defects in TMEM165 are associated with strong Golgi glycosylation abnormalities. Our previous work has shown that TMEM165 rapidly degrades with supraphysiological manganese supplementation. In this paper, we establish a functional link between TMEM165 and SPCA1, the Golgi Ca2+/Mn2+ P-type ATPase pump. A nearly complete loss of TMEM165 was observed in SPCA1-deficient Hap1 cells. We demonstrate that TMEM165 was constitutively degraded in lysosomes in the absence of SPCA1. Complementation studies showed that TMEM165 abundance was directly dependent on SPCA1's function and more specifically its capacity to pump Mn2+ from the cytosol into the Golgi lumen. Among SPCA1 mutants that differentially impair Mn2+ and Ca2+ transport, only the Q747A mutant that favors Mn2+ pumping rescues the abundance and Golgi subcellular localization of TMEM165. Interestingly, the overexpression of SERCA2b also rescues the expression of TMEM165. Finally, this paper highlights that TMEM165 expression is linked to the function of SPCA1.


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