Regulation of G proteins and adenylyl cyclase in brain regions of caffeine-tolerant and -dependent mice

Leite‐Morris, Kimberly A.; Kaplan, Gary B.; Smith, Jonathan G.; Sears, Mary T.

doi:10.1016/s0006-8993(98)00582-4

Cited by 9 publications

(4 citation statements)

References 37 publications

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“…Experiments in cortical cell cultures demonstrate that caffeine selectively injures neurons primarily through apoptosis regardless of excitotoxicity and oxidative stress, which is mediated through activation of caspase-3. In mice, systemic administration of caffeine at doses of 97, 125 or 194 mg/kg/day resulted in mean plasma concentration of caffeine up to 2.7, 4.9 and 7.1 mg/ml 7 days later: is comparable to that in human studies of chronic caffeine treatment [14][15][16][17]. In the present study, neonatal rats received i.p.…”

Section: Discussionsupporting

confidence: 75%

“…Further study will be needed to delineate upstream signals underlying caffeine-induced activation of caspase-3 that are classified into mitochondria-dependent intrinsic apoptotic pathways involving cytochrome c release from mitochondria and extrinsic apoptotic pathways involving interaction of Fas and Fas ligand [21,22]. Caffeine may trigger caspasedependent apoptosis possibly by interfering with activity of adenylate cyclase or intracellular Ca 2þ homeostasis that can cause neuronal cell apoptosis [6,14,23,24]. (c) Cortical cell cultures (DIV10^12) were exposed to 500 mM ca¡eine, alone or with10 mM MK-801 (MK), 50 mM CNQX,1 mg/ml cycloheximide (CHX), 25 mM Kþ,100 ng/ml BDNF or100 ng/ml insulin.…”

Section: Discussionmentioning

confidence: 99%

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Caffeine-induced neuronal death in neonatal rat brain and cortical cell cultures

Kang¹,

Lee²,

Won³

et al. 2002

NeuroReport

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We examined the potential neurotoxicity of ca¡eine in vivo and in vitro. Intraperitoneal administration of ca¡eine (50 mg/kg, 3 times a day) produced neuronal death in various brain areas of neonatal rats 24 h later. Ca¡eine at doses 4 300 mM was also neurotoxic in murine cortical cell cultures. Ca¡eine-induced neuronal death was accompanied by cell body shrinkage and attenuated by anti-apoptotic drugs including cycloheximide, high potassium, and growth factors. Two necrotic pathways, excitotoxicity and oxidative stress, did not mediate ca¡eine neurotoxicity. The pro-apoptotic protease caspase-3 was activated to mediate neuronal death following exposure to ca¡eine. The present ¢ndings suggest that ca¡eine may cause caspase-3-dependent neuronal cell apoptosis in neonatal rat as well as in vitro. NeuroReport 13:1945^1950

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Caffeine-induced neuronal death in neonatal rat brain and cortical cell cultures

Kang¹,

Lee²,

Won³

et al. 2002

NeuroReport

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“…Increased or unaltered ADORA1 mRNA expression has been reported in brain after long-term caffeine treatment ( 33 , 34 ). Other studies also found that short-term caffeine treatment reduces adenylyl cyclase activity, whereas chronic caffeine treatment results in increased adenylyl cyclase activity due to adaptation after caffeine intake ( 35 ). The decrease of ADORA1 expression observed in this study may be due to the short-term caffeine incubation.…”

Section: Discussionmentioning

confidence: 96%

Inhibition of Parathyroid Hormone Secretion by Caffeine in Human Parathyroid Cells

Farnebo

Bränström

2013

The Journal of Clinical Endocrinology & Metabolism

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Context and Objective:Caffeine is a highly consumed psychoactive substance present in our daily drinks. Independent studies have reported associations between caffeine consumption, low bone mineral density, and urinary calcium loss, as well as impaired bone development in vitro and in vivo. Calcium (Ca2+), vitamin D, and PTH are critical regulators of bone remodeling. A possible association between caffeine and parathyroid gland function has been suggested in the literature.Design, Setting, and Patients:Effects of caffeine on PTH secretion and Ca2+ levels were determined by batch incubation and Fura-2, respectively, in pathological parathyroid cells. Protein expressions were studied by Western blot and immunohistochemistry in normal and parathyroid adenoma tissues. Alterations in gene expressions of adenosine receptor A1 (ADORA1) and A2 (ADORA2A) and PTH were quantified by PCR; intracellular cAMP levels and protein kinase A activity were analyzed by an antibody-based assay.Results:We studied physiological concentrations of caffeine ranging from 1 to 50 μm and found that 50 μm caffeine caused a significant decrease of PTH secretion and PTH gene expression. This decrease occurred in parallel with a decrease of the intracellular cAMP level, protein kinase A activity, and ADORA1 gene expression, indicating a possible causal relationship. The intracellular level of Ca2+ was unaffected even by high concentrations of caffeine. Protein expressions demonstrated two main targets for caffeine—ADORA1 and ADORA2A.Conclusion:A physiological high dose of caffeine inhibits PTH secretion in human parathyroid cells, possibly due to a decrease of the intracellular level of cAMP. The observation demonstrates a functional link between caffeine and parathyroid cell function.

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“…31 A short-term CAF treatment is evident to reduce adenylyl cyclase activity in mouse model. 32 In a recent study, it has been seen that CAF intracts with the cAMP-induced chemotactic signal pathways in Dictyostelium, probably through multiple targets, including phosphoinositide 3-kinases (PI3K) and mammalian target of rapaycin complex 2 (mTORC2). 33 In this study, we have seen that CAF significantly (p< 0.05) increased the latent periods in diarrheal mice as compared to the VEH group.…”

Section: Discussionmentioning

confidence: 99%

Anti-diarrheal Activity of Caffeine: A Modulatory Effect with Loperamide and through 6FH5 (PIK3CG) Protein Interaction Pathway

Faria¹,

Hassan²,

Hossain³

et al. 2020

IJPER

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Regulation of G proteins and adenylyl cyclase in brain regions of caffeine-tolerant and -dependent mice

Cited by 9 publications

References 37 publications

Caffeine-induced neuronal death in neonatal rat brain and cortical cell cultures

Caffeine-induced neuronal death in neonatal rat brain and cortical cell cultures

Inhibition of Parathyroid Hormone Secretion by Caffeine in Human Parathyroid Cells

Anti-diarrheal Activity of Caffeine: A Modulatory Effect with Loperamide and through 6FH5 (PIK3CG) Protein Interaction Pathway

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