scholarly journals Paliperidone and aripiprazole differentially affect the strength of calcium-secretion coupling in female pituitary lactotrophs

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Marek Kucka ◽  
Melanija Tomić ◽  
Ivana Bjelobaba ◽  
Stanko S. Stojilkovic ◽  
Dejan B. Budimirovic
Keyword(s):  
Digestion ◽  
1983 ◽  
Vol 26 (2) ◽  
pp. 89-98 ◽  
Author(s):  
P. Layer ◽  
J. Hotz ◽  
H. Goebell
Keyword(s):  

Digestion ◽  
1985 ◽  
Vol 32 (1) ◽  
pp. 1-9 ◽  
Author(s):  
C. Boustière ◽  
H. Sarles ◽  
J. Lohse ◽  
J.P. Durbec ◽  
J. Sahel

2005 ◽  
Vol 10 (2) ◽  
pp. 119-128 ◽  
Author(s):  
Margaret C. Neville
Keyword(s):  

Gut ◽  
1981 ◽  
Vol 22 (5) ◽  
pp. 355-358 ◽  
Author(s):  
J E Clain ◽  
G O Barbezat ◽  
I N Marks

2015 ◽  
Vol 226 (1) ◽  
pp. 43-55 ◽  
Author(s):  
Jimena Laporta ◽  
Spencer A E Moore ◽  
Samantha R Weaver ◽  
Callyssa M Cronick ◽  
Megan Olsen ◽  
...  

A 4×4 Latin square design in which varied doses (0, 0.5, 1.0, and 1.5 mg/kg) of 5-hydroxy-l-tryptophan (5-HTP, a serotonin precursor) were intravenously infused into late-lactation, non-pregnant Holstein dairy cows was used to determine the effects of serotonin on calcium and energy metabolism. Infusion periods lasted 4 days, with a 5-day washout between periods. Cows were infused at a constant rate for 1 h each day. Blood was collected pre- and 5, 10, 30, 60, 90, and 120 min post-infusion, urine was collected pre- and post-infusion, and milk was collected daily. All of the 5-HTP doses increased systemic serotonin as compared to the 0 mg/kg dose, and the 1.0 and 1.5 mg/kg doses increased circulating glucose and non-esterified fatty acids (NEFA) and decreased beta-hydroxybutyrate (βHBA) concentrations. Treatment of cows with either 1.0 or 1.5 mg/kg 5-HTP doses decreased urine calcium elimination, and the 1.5 mg/kg dose increased milk calcium concentrations. No differences were detected in the heart rates, respiration rates, or body temperatures of the cows; however, manure scores and defecation frequency were affected. Indeed, cows that received 5-HTP defecated more, and the consistency of their manure was softer. Treatment of late-lactation dairy cows with 5-HTP improved energy metabolism, decreased loss of calcium into urine, and increased calcium secretion into milk. Further research should target the effects of increasing serotonin during the transition period to determine any benefits for post-parturient calcium and glucose metabolism.


1997 ◽  
Vol 64 (4) ◽  
pp. 633-636
Author(s):  
GORDON E. THOMPSON ◽  
S. KHAWAR ABBAS ◽  
CARL HOLT ◽  
ANTHONY D. CARE

During lactogenesis in the goat, the onset of secretion of calcium into milk occurs at parturition (Thompson et al. 1995) at approximately the same time as the onset of secretion of parathyroid hormone-related protein (PTHrP) by the mammary gland (Ratcliffe et al. 1992); these events may be unrelated or PTHrP may be involved in calcium transport from blood to milk.Parturition in goats is initiated by fetal secretion of cortisol (Flint et al. 1978) and maternal secretion of cortisol also increases (Paterson & Linzell, 1971). Injecting cortisol locally into the sinus of a mammary gland of the late-pregnant goat when the tight junctions between secretory epithelial cells appear to be ‘loose’, and injectate can reach the basolateral surfaces of secretory cells, stimulates an early tightening of these junctions (Thompson, 1996) as occurs naturally at parturition. This tightening can be produced by an increased concentration of ionized calcium in the extracellular fluid of the gland (Neville & Peaker, 1981).The experiments reported here were undertaken to determine if cortisol injection stimulates the mammary gland to secrete both PTHrP and calcium before parturition.


1994 ◽  
Vol 124 (5) ◽  
pp. 726-731 ◽  
Author(s):  
Peter D. O'Loughlin ◽  
Howard A. Morris

Author(s):  
David Shennan

AbstractThe secretion of calcium into milk by mammary epithelial cells is a fundamentally important process. Despite this, the mechanisms which underlie the movement of calcium across the lactating mammary gland are still poorly understood. There are, however, two models which describe the handling of calcium by mammary epithelial cells. On the one hand, a model which has existed for several decades, suggests that the vast majority of calcium enters milk via the Golgi secretory vesicle route. On the other hand, a new model has recently been proposed which implies that the active transport of calcium across the apical membrane of mammary secretory cells is central to milk calcium secretion. This short review examines the strengths and weaknesses of both models and suggests some experiments which could add to our understanding of mammary calcium transport.


1981 ◽  
Vol 241 (3) ◽  
pp. G215-G221
Author(s):  
M. J. Favus ◽  
M. Berelowitz ◽  
F. L. Coe

The addition of somatostatin (SRIF) to rat descending colon in vitro increased the calcium secretory flux from serosa to mucosa (Js leads to m) and reduced tissue short-circuit current (Isc) but did not alter the absorptive flux from mucosa to serosa (Js leads to m). Js leads to m increased by 37% at 10(-9) M SRIF and by 48% at 10(-6) M. The response to SRIF was not altered by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], and SRIF did not interfere with stimulation of calcium Jm leads to s by 1,25(OH)2D3. Removal of sodium from the buffer abolished the stimulation of Js leads to m by SRIF without reducing basal Js leads to m. Secretory fluxes of mannitol and calcium were strongly correlated in the presence and absence of SRIF, suggesting that SRIF stimulates a paracellular transepithelial pathway for calcium. In the duodenum, SRIF altered neither calcium Js leads to m nor Isc. In the ileum, calcium Js leads to m increased and Isc decreased, as in the colon, but only by 28 and 12%, respectively. The maximal change in calcium Js leads to m caused by SRIF in these three intestinal segments was negatively correlated with the tissue concentration of immunoreactive SRIF. These results suggest that intestinal calcium secretion could, in part, be regulated by intestinal SRIF.


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