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  • 1
    Electronic Resource
    Electronic Resource
    Chronic caffeine alters the density of adenosine, adrenergic, cholinergic, GABA, and serotonin receptors and calcium channels in mouse brain (1993)
    Springer
    Cellular and molecular neurobiology 13 (1993), S. 247-261 
    Details
    ISSN: 1573-6830
    Keywords: caffeine ; adenosine receptors ; adrenergic receptors ; cholinergic receptors ; serotonin receptors ; GABA receptors ; calcium channels ; dopamine receptors ; NMDA receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. Chronic ingestion of caffeine by male NIH strain mice alters the density of a variety of central receptors. 2. The density of cortical A1 adenosine receptors is increased by 20%, while the density of striatal A2A adenosine receptors is unaltered. 3. The densities of corticalβ 1 and cerebellarβ 2 adrenergic receptors are reduced byca. 25%, while the densities of corticalα 1 andα 2 adrenergic receptors are not significantly altered. Densities of striatal D1 and D2 dopaminergic receptors are unaltered. The densities of cortical 5 HT1 and 5 HT2 serotonergic receptors are increased by 26–30%. Densities of cortical muscarinic and nicotinic receptors are increased by 40–50%. The density of cortical benzodiazepine-binding sites associated with GABAA receptors is increased by 65%, and the affinity appears slightly decreased. The density of cortical MK-801 sites associated with NMDA-glutaminergic receptors appear unaltered. 4. The density of cortical nitrendipine-binding sites associated with calcium channels is increased by 18%. 5. The results indicate that chronic ingestion of caffeine equivalent to about 100 mg/kg/day in mice causes a wide range of biochemical alterations in the central nervous system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00733753
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  • 2
    Electronic Resource
    Electronic Resource
    The amphiphilic peptide adenoregulin enhances agonist binding to A1-adenosine receptors and [35S]GTPγS to brain membranes (1995)
    Springer
    Cellular and molecular neurobiology 15 (1995), S. 465-493 
    Details
    ISSN: 1573-6830
    Keywords: peptides ; adenosine receptors ; adrenergic receptors ; serotonin receptors ; guanyl nucleotide exchange
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. Adenoregulin is an amphilic peptide isolated from skin mucus of the tree frog,Phyllomedusa bicolor. Synthetic adenoregulin enhanced the binding of agonists to several G-protein-coupled receptors in rat brain membranes. 2. The maximal enhancement of agonist binding, and in parentheses, the concentration of adenoregulin affording maximal enhancement were as follows: 60% (20 µM) for A1-adenosine receptors, 30% (100 µM) for A2a-adenosine receptors, 20% (2 µM) forα 2-adrenergic receptors, and 30% (100 µM) for 5HT1A receptors. High affinity agonist binding for A1-,α 2-, and 5HT1A-receptors was virtually abolished by GTPγS in the presence of adenoregulin, but was only partially abolished in its absence. Magnesium ions increased the binding of agonists to receptors and reduced the enhancement elicited by adenoregulin. 3. The effect of adenoregulin on binding of N6-cyclohexyladenosine ([3H]CHA) to A1-receptors was relatively slow and was irreversible. Adenoregulin increased the Bmax value for [3H]CHA binding sites, and the proportion of high affinity states, and slowed the rate of [3H]CHA dissociation. Binding of the A1-selective antagonist, [3H]DPCPX, was maximally enhanced by only 13% at 2 µM adenoregulin. Basal and A1-adenosine receptor-stimulated binding of [35S]GTPγS were maximally enhanced 45% and 23%, respectively, by 50 µM adenoregulin. In CHAPS-solubilized membranes from rat cortex, the binding of both [3H]CHA and [3H]DPCPX were enhanced by adenoregulin. Binding of [3H]CHA to membranes from DDT1 MF-2 cells was maximally enhanced 17% at 20 µM adenoregulin. In intact DDT1 MF-2 cells, 20 µM adenoregulin did not potentiate the inhibition of cyclic AMP accumulation mediatedvia the adenosine A1 receptor. 4. It is proposed that adenoregulin enhances agonist binding through a mechanism involving enhancement of guanyl nucleotide exchange at G-proteins, resulting in a conversion of receptors into a high affinity state complexed with guanyl nucleotide-free G-protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02071881
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  • 3
    Electronic Resource
    Electronic Resource
    Chronic Effects of Xanthines on Levels of Central Receptors in Mice (1999)
    Springer
    Cellular and molecular neurobiology 19 (1999), S. 719-732 
    Details
    ISSN: 1573-6830
    Keywords: caffeine ; adenosine receptors ; adrenergic receptors ; serotonergic receptors ; cholinergic receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract 1.Chronic ingestion of caffeine causes a significant increase in levels of A1-adenosine, nicotinic and muscarinic receptors, serotonergic receptors, GABAA receptors and L-type calcium channels in cerebral cortical membranes from mice NIH Swiss strain mice. 2.Chronic theophylline and paraxanthine had effects similar to those of caffeine except that levels of L-type channels were unchanged. Chronic theobromine, a weak adenosine antagonist, and 1-isobutyl-3-methylxanthine (IBMX), a potent adenosine antagonist and phosphodiesterase inhibitor, caused only an increase in levels of A1-adenosine receptors. A combination of chronic caffeine and IBMX had the same effects on receptors as caffeine alone. Chronic 3,7-dimethyl-1-propargylxanthine (DMPX), a somewhat selective A2A-antagonist, caused only an increase in levels of A1-adenosine receptors. Pentoxyfylline, an adenosine-uptake inhibitor inactive at adenosine receptors, had no effect on receptor levels or calcium channels. 3.A comparison of plasma and brain levels of xanthines indicated that caffeine penetrated more readily and attained somewhat higher brain levels than theophylline or theobromine. Penetration and levels were even lower for IBMX, paraxanthine, DMPX, and pentoxyfylline. 4.The results suggest that effective blockade of both A1 and A2A-adenosine receptors is necessary for the full spectrum of biochemical changes elicited by chronic ingestion of xanthines, such as caffeine, theophylline, and paraxanthine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006901005925
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  • 4
    Electronic Resource
    Electronic Resource
    Subclasses of adenosine receptors in the central nervous system: Interaction with caffeine and related methylxanthines (1983)
    Springer
    Cellular and molecular neurobiology 3 (1983), S. 69-80 
    Details
    ISSN: 1573-6830
    Keywords: caffeine ; methylxanthines ; adenosine receptors ; adenylate cyclase ; brain ; striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. The potencies of caffeine and related methylxanthines as adenosine antagonists were assessed with respect to three apparent subtypes of adenosine receptors in rat brain preparations: (i) the A1-adenosine receptor which binds with a very high affinity the ligand [3H]cyclohexyladenosine (K D, 1 nM) in rat brain membranes; (ii) a ubiquitous low-affinity A2-adenosine receptor which activates cyclic AMP accumulation in rat brain slices—this A2-adenosine system exhibits an EC50 for 2-chloroadenosine of about 20µM; and (iii) a relatively high-affinity A2-adenosine receptor which activates adenylate cyclase in rat striatal membranes—this A2-adenosine system exhibits an EC50 for 2-chloroadenosine of about 0.5µM and is present in striatal but not in cerebral cortical membranes. 2. The rank order of potency for methylxanthines versus binding of 1 nM [3H]cyclohexyladenosine in membranes from eight rat brain regions is theophylline (IC50, 20–30µM) 〉 paraxanthine (IC50, 40–65µM) 〉 caffeine (IC50, 90–110µM) 〉 theobromine (IC50, 210–280µM). There thus appears to be little difference in A1-receptors in different brain regions in terms of interaction with these methylxanthines. 1-Methylxanthine is more potent than caffeine in rat cerebral cortical membranes, while 3-methylxanthine and 7-methylxanthine are less potent than caffeine. 3. The rank order of potency for methylxanthines versus activation of cyclic AMP accumulation by 50µM 2-chloroadenosine in rat striatal slices is theophylline (IC50, 60µM) 〉 paraxanthine (IC50, 90µM) 〉 caffeine (IC50, 120µM) » theobromine (IC50, 〉 1000µM). Similar potencies pertain in cerebral cortical slices. 4. The rank order of potency of methylxanthines versus activation of adenylate cyclase by 1µM 2-chloroadenosine in rat striatal membranes is theophylline (IC50, 20µM) 〉 paraxanthine (IC50, 40µM) 〉 caffeine (IC50, 80µM) » theobromine (IC50, 〉 1000µM). 5. Caffeine and other methylxanthines, thus, antagonize effectively both A1- and A2-adenosine receptors in brain perparations. Theobromine appears less effective versus A2-receptors than versus A1-receptors. Caffeine exhibits aK i value of about 50µM at the very high-affinity A1-binding sites, aK i value of about 30µM at the low-affinity A2-adenosine site in brain slices, and aK i value of about 27µM at the high-affinity A2-adenosine site in striatal membranes. The functional significance of antagonism of such adenosine receptors by caffeinein situ will depend both on the local levels of adenosine and on the affinity for adenosine for the receptor, since antagonism by xanthines is competitive in nature. In addition, the functional significance of xanthine action will depend on the degree of inhibition of adenosine input which is required to alter the output signal. For a stimulatory input to adenylate cyclase via an A2-adenosine receptor, profound antagonism by methylxanthines is probably required to alter the cyclic AMP-mediated output signal, while for inhibitory input to adenylate cyclase via an A1-adenosine receptor, presumably a lesser degree of antagonism by methylxanthines may be required to alter the cyclic AMP-mediated output signal.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00734999
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