2015
DOI: 10.1155/2015/872684
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Abstract: Adenosine A1 and cannabinoid CB1 receptors are highly expressed in hippocampus where they trigger similar transduction pathways. We investigated how the combined acute activation of A1 and CB1 receptors modulates cAMP accumulation in rat hippocampal slices. The CB1 agonist WIN55212-2 (0.3–30 μM) decreased forskolin-stimulated cAMP accumulation with an EC50 of 6.6 ± 2.7 μM and an E max⁡ of 31% ± 2%, whereas for the A1 agonist, N6-cyclopentyladenosine (CPA, 10–150 nM), an EC50 of 35 ± 19 nM, and an E max⁡ of 29%… Show more

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Cited by 10 publications
(7 citation statements)
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“…in agreement with previous studies where acute co-activation of adenosine A1 and cannabinoid CB1 receptor have been shown to generate additive effects in inhibiting glutamatergic synaptic transmission and cAMP formation in the rat hippocampus (Serpa et al, 2009(Serpa et al, , 2015.…”
Section: Discussionsupporting
confidence: 93%
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“…in agreement with previous studies where acute co-activation of adenosine A1 and cannabinoid CB1 receptor have been shown to generate additive effects in inhibiting glutamatergic synaptic transmission and cAMP formation in the rat hippocampus (Serpa et al, 2009(Serpa et al, , 2015.…”
Section: Discussionsupporting
confidence: 93%
“…Given the similarity between transducing pathways operated by adenosine A1 and cannabinoid CB1 receptors, as well as the identical effects produced by both receptors on nerve cells, clarification of the combined activity of these receptors is particularly relevant, since the harmful effects of neurotoxic insults might be cumulatively dampened. Previous studies showed that acute co-activation of adenosine A1 and cannabinoid CB1 receptors generates additive effects when inhibiting excitatory synaptic transmission and cAMP formation in the rat hippocampus (Serpa et al, 2009(Serpa et al, , 2015. We now further tested how the combined action of A1 and CB1 receptor agonists modulates NMDA-mediated excitotoxic insult at the rat organotypic hippocampal slice.…”
Section: Introductionmentioning
confidence: 94%
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“…Adenosine plays a regulatory role in the nervous system by decreasing neurotransmitter release and synaptic transmission, including excitatory synaptic transmission (Dias, Rombo, Ribeiro, Henley, & Sebastião, ; Dunwiddie & Hoffer, ; Pinto, Serpa, Sebastião, & Cascalheira, ; Serpa, Ribeiro, & Sebastião, ), protecting against neurotoxic insults (Ribeiro, Sebastião, & Mendonça, ; Serpa, Pinto, Bernardino, & Cascalheira, ) and modulating synaptic plasticity (Dias et al, ; Santschi, Zhang, & Stanton, ). Most of these adenosine actions are mediated by activation of G‐protein‐coupled adenosine receptors located at the extracellular membrane, specifically A 1 , A 2A , A 2B and A 3 receptors (Dias et al, ; Serpa, Sara, Ribeiro, Sebastião, & Cascalheira, ; Serpa, Sebastião, & Cascalheira, ). However, adenosine may play relevant adenosine receptor‐independent functions, such as modulation of epigenetic processes (Boison, Sandau, Ruskin, Kawamura, & Masino, ; Williams‐Karnesky et al, ).…”
Section: Introductionmentioning
confidence: 99%
“…Adenosine A1 receptor (AA1R) in the adenosine receptor family is widely present in the CNS, especially with high expressions in the cerebral cortex and hippocampus 5 , exerting brain protective and antiepileptic effects, mainly by binding corresponding G proteins. If exogenous drugs are used to activate AA1R or to increase the concentration of endogenous adenosine, AA1R can protect the brain and combat epilepsy, but the underlying mechanisms are still largely unknown [6][7][8] . Epileptic seizures are closely related to neuronal apoptosis.…”
Section: Introductionmentioning
confidence: 99%