scholarly journals Plasma calcium concentration during detoxification predicts neural cue-reactivity and craving during early abstinence in alcohol-dependent patients

Author(s):  
Patrick Bach ◽  
Rilana Schuster ◽  
Anne Koopmann ◽  
Sabine Vollstaedt-Klein ◽  
Rainer Spanagel ◽  
...  

AbstractRecent studies on the pathophysiology of alcohol dependence suggest a link between peripheral calcium concentrations and alcohol craving. Here, we investigated the association between plasma calcium concentration, cue-induced brain activation, and alcohol craving. Plasma calcium concentrations were measured at the onset of inpatient detoxification in a sample of N = 115 alcohol-dependent patients. Alcohol cue-reactivity was assessed during early abstinence (mean 11.1 days) using a functional magnetic resonance imaging (fMRI) alcohol cue-reactivity task. Multiple regression analyses and bivariate correlations between plasma calcium concentrations, clinical craving measures and neural alcohol cue-reactivity (CR) were tested. Results show a significant negative correlation between plasma calcium concentrations and compulsive alcohol craving. Higher calcium levels predicted higher alcohol cue-induced brain response in a cluster of frontal brain areas, including the dorsolateral prefrontal cortex (dlPFC), the anterior prefrontal cortex (alPFC), and the inferior (IFG) and middle frontal gyri (MFG). In addition, functional brain activation in those areas correlated negatively with craving for alcohol during fMRI. Higher peripheral calcium concentrations during withdrawal predicted increased alcohol cue-induced brain activation in frontal brain areas, which are associated with craving inhibition and cognitive control functions. This might indicate that higher plasma calcium concentrations at onset of detoxification could modulate craving inhibition during early abstinence.Trial registration number: DRKS00003388; date of registration: 14.12.2011.

2011 ◽  
Vol 26 (S2) ◽  
pp. 1913-1913
Author(s):  
A. Beck ◽  
T. Wüstenberg ◽  
J. Wrase-Post ◽  
F. Schlagenhauf ◽  
S. Vollstädt-Klein ◽  
...  

IntroductionIn alcoholism, one relevant mechanism contributing to relapse is the exposure to stimuli that are associated with alcohol intake. Such conditioned cues can elicit conditioned responses like alcohol craving and consumption. In the last decade, considerable progress has been made in identifying basic neuronal mechanisms that underlie cue-induced alcohol craving.Objectives/ aimsWe explored whether functional brain activation during exposure to alcohol-associated stimuli is related to the prospective relapse risk in detoxified alcohol-dependent patients.Methods46 alcohol-dependent and 46 healthy volunteers participated in a fMRI study using a cue reactivity paradigm, in which visual alcohol-related and control stimuli were presented. Patients were followed for 3 months. Afterwards data was analysed regarding the subsequent relapse, resulting in 16 abstainers and 30 relapsers.ResultsAlcohol-related versus neutral stimuli activated a frontocortical-limbic network including inferior, medial and middle frontal gyrus as well as putamen in the group of patients relative to healthy controls. Moreover, abstainers showed a stronger activation in orbitofrontal cortex as well as midbrain during the presentation of alcohol-related cues whereas relapsers revealed a stronger activation of cingulate gyrus.ConclusionsThis study suggests that cue-induced activation of orbitofrontal cortex and dopaminergic innervated midbrain is negatively associated with the prospective relapse risk in alcohol-dependent patients. This could indicate a more pronounced and conscious processing of alcohol cues which might serve as a warning signal and a behavioural controlling function. In contrast, prospective relapsers showed a stronger activation of cingulate gyrus, a region involved in the attribution of motivational value.


1970 ◽  
Vol 64 (1) ◽  
pp. 150-158 ◽  
Author(s):  
S. Pors Nielsen

ABSTRACT Intravenous infusion of isotonic magnesium chloride into young cats with a resultant mean plasma magnesium concentration of 7.7 meq./100 g protein was followed by a significant lowering of the plasma calcium concentration in 90 minutes. The rate of decrease of plasma calcium is consistent with the hypothesis that calcitonin is released by magnesium in high concentrations. There was no decrease in the plasma calcium concentration in cats of the same weight thyroparathyroidectomized 60 min before an identical magnesium chloride infusion or an infusion of isotonic sodium chloride at the same flow rate. The hypercalciuric effect of magnesium could not account for the hypocalcaemic effect of magnesium. Plasma magnesium concentration during magnesium infusion into cats with an intact thyroid-parathyroid gland complex was slightly, but not significantly higher than in acutely thyroparathyroidectomized cats.


1984 ◽  
Vol 67 (6) ◽  
pp. 613-618 ◽  
Author(s):  
B. F. Robinson ◽  
R. J. W. Phillips

1. The effect of a small increase in local plasma calcium concentration on the responsiveness of the forearm resistance vessels to verapamil has been examined in normal subjects, by using a plethysmographic method with infusion of calcium and other agents into the brachial artery. 2. Infusion of calcium at a rate which increased the concentration in forearm venous blood by about 0.5 mmol/l caused basal blood flow to fall by 19% and the dilator response to verapamil to fall by 35% (n = 8; P<0.02). 3. When, after 46 min, the infusion of calcium was discontinued, the dilator response to verapamil increased to reach a level 53% higher than the initial control (n = 8; P<0.02). 4. Infusion of calcium had no effect on the dilator response to sodium nitroprusside. 5. Infusion of noradrenaline at a rate which caused a greater reduction in basal flow than that induced by calcium had no effect on the response to verapamil. 6. It is concluded that the dilator response to verapamil, which is thought to reflect activity of the potential operated system for calcium entry, is selectively depressed by a small elevation of plasma calcium concentration, but subsequently becomes elevated. These findings point to an important role for calcium in the regulation of membrane function in the resistance vessels and support the view that altered calcium handling may contribute to the development of primary hypertension.


1983 ◽  
Vol 244 (4) ◽  
pp. E313-E316
Author(s):  
E. Hefti ◽  
U. Trechsel ◽  
H. Fleisch ◽  
J. P. Bonjour

The influence of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] treatment on the daily fluctuation of plasma calcium concentration ( [Ca]P1) in relation to the feeding-fasting alternation has been studied in vitamin D-replete sham-operated (sham) and thyroparathyroidectomized (TPTX) rats fed a normal Ca diet. 1,25(OH)2D3 was given (26 or 39 pmol/day) intraperitoneally either by single injection or constant infusion using osmotic minipumps. After 7 days of treatment [Ca]P1 was measured at 4-h intervals for 24 h. Pair-fed, sham and TPTX animals received the solvent vehicle intraperitoneally. The results show that in sham rats the very moderate daily fluctuation of [Ca]P1 was not accentuated by 1,25(OH)2D3. A marked fluctuation of [Ca]P1 in relation to the food intake was observed in untreated TPTX as compared with sham rats. In TPTX rats 1,25(OH)2D3 increased the fasting [Ca]P1. In contrast the rise in [Ca]P1 during feeding was not significantly accentuated by 1,25(OH)2D3. The daily fluctuation of [Ca]P1 was the same whether the dose of 1,25(OH)2D3 was given in one single injection or by constant infusion, suggesting that this hormone is not involved in the hour-to-hour regulation of [Ca]P1. In conclusion, in the absence of parathyroid glands, 1,25(OH)2D3 given in doses that stimulate intestinal calcium absorption has a much more pronounced effect on the fasting calcemia than on the rise in calcemia observed during the feeding period. These results suggest that the mobilization of calcium from bone could play an important role in the calcemic effect of 1,25(OH)2D3 when given in the hypoparathyroid state.


1974 ◽  
Vol 62 (3) ◽  
pp. 451-462 ◽  
Author(s):  
N. H. HUNT ◽  
A. D. PERRIS

SUMMARY Circadian changes in mitotic activity in rat bone marrow and thymus have been demonstrated to closely parallel variations in total and ionized calcium concentrations in plasma. These fluctuations in plasma calcium concentration and tissue mitosis were abolished by parathyroidectomy. Significant changes in plasma phosphate and magnesium concentrations were also observed over the 24 h period. The evidence suggests that hour-to-hour variations in the systems controlling calcium homeostasis determine the levels of mitosis in rat bone marrow and thymus.


1958 ◽  
Vol 37 (6) ◽  
pp. 1325-1328 ◽  
Author(s):  
Charles M. Winget ◽  
Arthur H. Smith ◽  
George N. Hoover

1980 ◽  
Vol 238 (6) ◽  
pp. E573-E578 ◽  
Author(s):  
G. A. Quamme

Renal calcium and magnesium reabsorption was investigated in young, thyroparathyroidectomized rats receiving synthetic salmon calcitonin. Kidney and tubular function was assessed by clearance and in vivo microperfusion techniques, respectively. Calcitonin reduced urinary calcium and magnesium excretion that was attributed to increased reabsorption within the loop of Henle. This enchanced reabsorption was independent of parathyroid hormone; however, it is contingent on a decline in plasma calcium concentration. Prevention of hypocalcemia by CaCl2 infusion in rats acutely administered calcitonin resulted in loop function comparable to animals not receiving the hormone. Calcitonin had little effect on proximal tubule or distal tubule electrolyte reabsorption. These results are consistent with a transport model for calcium and magnesium in the loop of Henle involving a contraluminal transfer step modulated by absolute extracellular calcium or magnesium. Furthermore, these studies suggest that the discrepancies present in the literature concerning renal effects of calcitonin on electrolyte reabsorption are due to variations in observed hormone action, namely, the effect on plasma calcium concentration.


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