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Neuroendocrinology. 2000 Oct;72(4):242-51.
Recruitment of calcium from intracellular stores does not occur during the expression of large spontaneous calcium oscillations in GH(3) cells and lactotropic cells in primary culture.

Zimber MP, Simasko SM.

Program in Neuroscience, Department of VCAPP, College of Veterinary Medicine, Washington State University, Pullman, WA 99164-6520, USA.

We used simultaneous electrophysiological and intracellular calcium microfluorometry recordings to directly test for the presence of a calcium-induced calcium release mechanism in individual GH(3) cells and cells of a lactotrope-enriched primary culture. In voltage-pulse experiments, extending the duration of a depolarizing voltage-pulse increased intracellular calcium concentration ([Ca(2+)](i)), but we did not observe any evidence for recruitment of intracellular calcium stores. Furthermore, depletion of intracellular calcium stores with thapsigargin or caffeine did not change the calculated calcium buffer capacity of the cells. In current-clamp experiments, we observed elevations in [Ca(2+)](i) in response to spontaneous action potentials. These [Ca(2+)](i) responses were not inhibited by thapsigargin or caffeine. We did find a significant correlation between the magnitude of spontaneous [Ca(2+)](i) increases and action potential duration. We conclude that intracellular calcium stores are not released during the spontaneous [Ca(2+)](i) oscillations observed in these cells, and that the magnitude of [Ca(2+)](i) oscillations is a direct result of extracellular calcium influx that is determined in part by action potential duration. 2000 S. Karger AG, Basel

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11070428&dopt=Abstract

Neurochem Res. 2000 Nov;25(11):1457-63.
Long-term caffeine inhibits Ehrlich ascites carcinoma cell-induced induction of central GABAergic activity.

Mukhopadhyay S, Poddar MK.

Department of Biochemistry, University of Calcutta, India.

Long-term administration (for 22-27 consecutive days) of caffeine (20 mg/kg/day p.o) developed tolerance to this drug by upregulating the central GABAergic activity. Development of Ehrlich ascites carcinoma (EAC) cell induced the whole brain GABAergic activity. But pretreatment of caffeine and continuation of its treatment in the course of development of EAC cells restored the EAC cell-induced change of GABAergic activity to control values. Thus, it may be concluded that caffeine (adenosine receptor antagonist) suppresses the EAC cell-induced induction of whole brain GABAergic activity in mice.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11071364&dopt=Abstract

Prev Med. 2000 Nov;31(5):562-8.
Is caffeine associated with bone mineral density in young adult women?

Conlisk AJ, Galuska DA.

Biological and Biomedical Sciences Division, Nutrition and Health Sciences Program, Emory University, Atlanta, Georgia 30322, USA. aconlimory.edu

BACKGROUND: By increasing the urinary excretion of calcium, caffeine consumption may reduce bone mineral density (BMD) and subsequently increase the risk for osteoporotic fracture. Although negative associations between caffeine consumption and BMD have been reported for postmenopausal women, in particular for those who consume low amounts of dietary calcium, the relation between caffeine and BMD in younger women is unclear. Therefore, we evaluated the association between caffeine consumption and BMD in a cross-sectional study of 177 healthy white women, age 19-26 years, who attended a Midwestern university. METHODS: Average caffeine intake (milligrams per day) was calculated from self-reports of the consumption of coffee, decaffeinated coffee, tea, colas, chocolate products, and select medications during the previous 12 months (mean caffeine intake = 99. 9 mg/day). BMD (grams per square centimeter) at the femoral neck and the lumbar spine was measured by dual-energy X-ray absorptiometry. RESULTS: After adjusting in linear regression models for potential confounders, including height, body mass index, age at menarche, calcium intake, protein consumption, alcohol consumption, and tobacco use, caffeine consumption was not a significant predictor of BMD. For every 100 mg of caffeine consumed, femoral neck BMD decreased 0.0069 g/cm(2) (95% confidence in terval [CI] = -0.0215, 0. 0076) and lumbar spine BMD decreased 0.0119 g/cm(2) (95% CI = -0. 0271, 0.0033). No single source of caffeine was significantly associated with a decrease in BMD. Furthermore, the association between caffeine consumption and BMD at either site did not differ significantly between those who consumed low levels of calcium (< or =836 mg/day) and those who consumed high levels of calcium (>836 mg/day). CONCLUSIONS: Caffeine intake in the range consumed by young adult women is not an important risk factor for low BMD. 2000 American Health Foundation and Academic Press.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11071837&dopt=Abstract

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