Caffeine inhibits forskolin-stimulated cyclic AMP accumulation in rat brain

Mante, Saakwa; Minneman, Kenneth P.

doi:10.1016/0014-2999(90)90231-t

Cited by 8 publications

(5 citation statements)

References 6 publications

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“…In agreement with the results obtained in slice preparation from mammalian and teleost brain (Mante and Minneman 1990;De Lapp and Eckols 1992;Lucchi et al 1994), 10-5 M forskolin caused a strong accumulation of cAMP in eel synaptosomal preparation. 10 -4 M CHA decreased cyclic AMP levels and this effect was antagonized by CPT.…”

Section: 5-supporting

confidence: 80%

Biochemical and pharmacological characterization of adenosine A1 receptors in eel (Anguilla anguilla) brain

Poli

Pavan

Lucchi

et al. 1997

Fish Physiol Biochem

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N 6 -cyclohexyl[3H]adenosine ([ 3 H]CHA) was used to label adenosine Al receptors in membranes prepared from male and female eel whole brain. The Al receptor agonist [ 3 H]CHA bound saturably, reversibly and with high affinity (Kd = 0.91 ± 0.12 nM; Bma = 120.36 5.2 fmol mg 1 protein). In equilibrium competition experiments, the adenosine agonists and antagonists all displaced [ 3 H]CHA from high-affinity binding sites with the rank order of potency in displacing, characteristics of an Al adenosine receptor. Mg 2 ' dramatically increased the affinity of [ 3 H]CHA without modifying the maximal binding capacity. The specific binding was inhibited by guanosine 5'-triphosphate (K i = 2.54 i 0.98 M). The [ 3 H]CHA binding sites are ubiquitously distributed with a maximum in cerebellum and a minimum in olfactory bulb. No difference was observed between male and female brain. In eel brain, synaptosomes (P2), stimulation of adenosine 3',5'-monophosphate (cyclic AMP) accumulation with 10 -5 M forskolin was markedly reduced (45.5%) by treatment with the adenosine Al receptor agonist CHA (10 -M), and the reduction was reversed in presence of the selective Al receptor antagonist 8-cyclopentyltheophylline (10-5 M). In superfused eel cerebellar synaptosomes, K + stimulated the release of adenosine in a partially Ca 2 +-dependent manner. The findings, taken together, suggest the hypothesis that adenosine Al receptors present in eel brain could modulate synaptic transmission, as Al receptors do in other vertebrates.

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Section: 5-supporting

confidence: 80%

Biochemical and pharmacological characterization of adenosine A1 receptors in eel (Anguilla anguilla) brain

Poli

Pavan

Lucchi

et al. 1997

Fish Physiol Biochem

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“…They point out that 200fold as much ADA was required to inhibit the F response as was needed to block cAMP accumulation due to added 100 pM adenosine. Stimulation of CAMP accumulation in cortex slices by adenosine and its analogue occurs through the low-affinity A z~ receptor and requires concentrations of greater than 10 pM (Bazil and Minneman, 1986;Bruns et al, 1986;Mante and Minneman, 19906; this study, Fig. 3).…”

Section: Discussionmentioning

confidence: 62%

“…Recently, inhibition of F-stimulated cAMP accumulation in rat cortex slices by caffeine (CAF) was reported (Mante and Minneman, 1990a). These authors investigated the role of endogenous adenosine in this response and concluded that most of the F stimulation observed was not due to endogenous adenosine and that CAF inhibition of F stimulation was largely due to some mechanism other than adenosine receptor blockade (Mante and Minneman, 1990b).…”

mentioning

confidence: 99%

Forskolin Stimulation of Cyclic AMP Accumulation in Rat Brain Cortex Slices Is Markedly Enhanced by Endogenous Adenosine

DeLapp

Eckols

1992

Journal of Neurochemistry

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Stimulation of cyclic AMP (cAMP) accumulation in rat cortex slices by 1 microM forskolin (F) was markedly reduced (96%) by treatment with adenosine deaminase (ADA). The effect of ADA was progressively less at higher concentrations of F, but still inhibited the response by 50% at 100 microM F. ADA-mediated inhibition of the cAMP response to 1 microM F was completely reversed by 5 microM 2-chloroadenosine (CA), an ADA-resistant analogue. Stimulation by F (controls) and F plus CA (ADA treated) in cortex slices was significantly inhibited by 200 microM caffeine (CAF) and by 10 microM 8-phenyltheophylline. cAMP accumulation in ADA-treated cortex slices stimulated with CA at concentrations from 5 to 100 microM was markedly enhanced by 1 microM F. Neither ADA treatment nor 200 microM CAF significantly affected cAMP accumulation in slices stimulated by 1 microM vasoactive intestinal polypeptide or adenylate cyclase in membranes stimulated by 1 microM F. CAF (1 mM) did not significantly increase basal cAMP levels in cortex slices, whereas 1 mM 3-isobutyl-1-methylxanthine caused a significant 80% increase and 100 microM rolipram enhanced cAMP levels by 4.5-fold. F-stimulated cAMP accumulation (1 microM) in cortex slices was inhibited 98% by 1 mM CAF and 49% by 1 mM 3-isobutyl-1-methylxanthine, and was enhanced 2.5-fold by 100 microM rolipram. These data have been interpreted to indicate that the stimulation of cAMP accumulation in rat cortex slices by 1 microM F is predominantly due to synergistic interaction with endogenous adenosine and that the inhibition of this response by CAF is largely due to blockade of adenosine receptors.

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“…Stimulation of cAMP formation by forskolin in brain slices is in part mediated by the endogenous adenosine acting at A2 purinergic receptors (Mante andMinneman. 1990: DeLapp andEckols, 1992).…”

Section: Resultsmentioning

confidence: 99%

Developmental Changes in the Modulation of Cyclic AMP Formation by the Metabotropic Glutamate Receptor Agonist 1S,3R‐Aminocyclopentane‐1,3‐Dicarboxylic Acid in Brain Slices

Casabona

Genazzani

Stefano

et al. 1992

Journal of Neurochemistry

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Metabotropic glutamate receptors (mGluRs) have been recently described as a family of guanine nucleotide-binding regulatory protein-coupled receptors with multiple signal transduction pathways. At least one of these receptors appears to be negatively coupled to adenylyl cyclase when stably expressed in transfected cells. We have studied how activation of native mGluRs modulates cyclic AMP (cAMP) formation in brain slices prepared from rats at different ages. 1S,3R-1-Aminocyclopentane-1,3-dicarboxylic acid (1S,1R-ACPD), a selective agonist of mGluRs, slightly increased basal cAMP formation but reduced forskolin-stimulated cAMP formation in adult hippocampal slices, in agreement with previous results. The action of 1S,3R-ACPD on basal cAMP formation was not reproduced by the ionotropic receptor agonists N-methyl-D-aspartate, kainate, and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate and was antagonised by L-2-amino-3-phosphonopropionate (L-AP-3). L-AP-3, however, did not prevent but rather mimicked the inhibitory action of 1S,3R-ACPD on forskolin-stimulated cAMP formation. In hippocampal slices from 1-, 8-, or 15-day-old rats, 1S,3R-ACPD increased basal cAMP formation but failed to reduce the action of forskolin. A similar development pattern of modulation was observed in hypothalamic slices with the difference that 1S,3R-ACPD did not stimulate basal cAMP formation in the hypothalamus of adult animals. These results suggest that inhibition of forskolin-stimulated cAMP formation by 1S,3R-ACPD is mediated by a specific mGluR subtype that is preferentially expressed in the adult.

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Caffeine inhibits forskolin-stimulated cyclic AMP accumulation in rat brain

Cited by 8 publications

References 6 publications

Biochemical and pharmacological characterization of adenosine A1 receptors in eel (Anguilla anguilla) brain

Biochemical and pharmacological characterization of adenosine A1 receptors in eel (Anguilla anguilla) brain

Forskolin Stimulation of Cyclic AMP Accumulation in Rat Brain Cortex Slices Is Markedly Enhanced by Endogenous Adenosine

Developmental Changes in the Modulation of Cyclic AMP Formation by the Metabotropic Glutamate Receptor Agonist 1S,3R‐Aminocyclopentane‐1,3‐Dicarboxylic Acid in Brain Slices

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