Effects of acute microinjections of thyroid hormone to the preoptic region of hypothyroid adult male rats on sleep, motor activity and body temperature

2013 ◽  
Vol 1516 ◽  
pp. 55-65 ◽  
Author(s):  
Steven X. Moffett ◽  
Phillip F. Giannopoulos ◽  
Thomas D. James ◽  
Joseph V. Martin
2013 ◽  
Vol 1516 ◽  
pp. 45-54 ◽  
Author(s):  
Joseph V. Martin ◽  
Phillip F. Giannopoulos ◽  
Steven X. Moffett ◽  
Thomas D. James

1993 ◽  
Vol 265 (2) ◽  
pp. F323-F326 ◽  
Author(s):  
K. W. Beers ◽  
T. P. Dousa

In our previous studies we established that thyroid hormones [L-thyroxine (T4) or 3,5,3'-triiodothyronine (T3)] elicit an increase in Na(+)-Pi symport in rat and mouse renal brush-border membrane (BBM) vesicles (BBMV), but the Na(+)-coupled symports of other solutes were not influenced. However, a recent report [H. S. Tenenhouse, J. Lee, and N. Harvey. Am. J. Physiol. 261 (Renal Fluid Electrolyte Physiol. 30): F420-F426, 1991]claimed that T3 increases to a similar degree both Na(+)-Pi symport and Na(+)-SO4 symport in murine renal BBM. Adult male rats were fed either normal (0.7% Pi; NPD) or high-phosphate (1.4% Pi; HPD) diet and received T3 (0.2 mg/100 g body wt ip) for 3 days before the kidneys were removed, BBMV were prepared, and the transport rates were determined. Although the Na(+)-Pi symport significantly increased (delta = +35%) in both NPD and HPD rats treated with T3, the Na(+)-35SO4 symport and Na(+)-D-[3H]glucose symports were not influenced by T3. Furthermore, treatment of NPD-fed mice with T3 using a similar protocol as rats resulted in a significant increase (delta = +26%) of Na(+)-(Pi)4 symport, but did not alter Na(+)-SO4 symport or Na(+)-glucose symport. Our findings thus document that T3 regulates selectively the Na(+)-Pi symporter in BBM without having any effect on other major divalent anions, such as SO4.


2000 ◽  
Vol 279 (3) ◽  
pp. R960-R965 ◽  
Author(s):  
S. M. Martin ◽  
B. C. Wilson ◽  
X. Chen ◽  
Y. Takahashi ◽  
P. Poulin ◽  
...  

Previous studies suggested that peripheral immune mediators may involve intermediates acting on the vagus nerve, such as CCK or serotonin (5-HT). We have therefore investigated a possible role for vagal CCK-A and 5-HT3receptors in the febrile response after intraperitoneal human recombinant interleukin-1β (IL-1β) or lipopolysaccharide (LPS). Unanesthetized, adult male rats instrumented with abdominal thermistors were given intraperitoneal CCK-8 sulfate (100 or 150 μg/kg) or 2-methyl-5-hydroxytryptamine maleate (4 mg/kg). In other experiments, rats were treated with either antagonists to the 5-HT3 receptor (ondansetron HCl; 100 μg/kg) or the CCK-A receptor (L-364,718, 100 or 200 μg/kg) in combination with LPS or IL-1β. CCK administration caused a short-lived hypothermia, but interference with the action of endogenous CCK at CCK-A receptors was without effect on IL-1β- or LPS-induced fever. Neither activation of 5-HT3 receptors nor blockade of 5-HT3 receptors affected body temperature or LPS fever. Taken together, our data support the idea that vagal afferents responsive to pyrogenic cytokines may be different from those responsive to CCK or 5-HT.


Life Sciences ◽  
2018 ◽  
Vol 192 ◽  
pp. 253-258 ◽  
Author(s):  
Fernanda Prieto-Almeida ◽  
Ana Carolina Panveloski-Costa ◽  
Fernanda Crunfli ◽  
Silvania da Silva Teixeira ◽  
Maria Tereza Nunes ◽  
...  

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