Effects of adenosine A1 and A2A receptor activation on the evoked release of glutamate from rat cerebrocortical synaptosomes
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The effects of adenosine A 2A and A 1 receptor activation on the release of glutamate were studied in rat cerebral cortex synaptosomes exposed in superfusion to adenosine receptor ligands. Adenosine (0.1 μ M) produced a significant potentiation of the Ca 2+‐dependent K+(15 m M)‐evoked [3 H]‐D‐aspartate overflow (20.4±3.5%), which was blocked by A 2A blocker SCH58261 (0.1 μ M). At higher concentrations (10 – 1000 μ M) adenosine inhibited in a DPCPX‐sensitive manner the Ca 2+‐dependent K+‐evoked [3 H]‐D‐aspartate overflow. The inhibitory effect of adenosine at 1000 μ M was significantly increased by SCH58261. This inhibition was antagonized by 1 μ M DPCPX. Adenosine did not produce any effect on basal release. The A 2A receptor agonist CGS 21680 was ineffective on basal release, but stimulated the Ca 2+‐dependent K+‐evoked overflow of [3 H]‐D‐aspartate (EC 50 ≃ 1 p M). The effect of 0.01 n M CGS 21680 was totally sensitive to the A 2A receptor antagonist SCH58261 (IC 50 ≃5 n M). The A 1 receptor agonist CCPA inhibited the Ca 2+‐dependent K+‐evoked [3 H]‐D‐aspartate overflow (EC 50 ≃ 20 n M). The effect of 100 n M CCPA was abolished by 100 n M of the A 1 receptor antagonist DPCPX. The K+(15 m M)‐evoked overflow of endogenous glutamate was enhanced by CGS 21680 (0.01 n M) and inhibited by CCPA (0.1 μ M). The effect of CGS 21680 was abolished by SCH58261 (0.1 μ M) and that of CCPA by DPCPX (0.1 μ M). It is concluded that adenosine and adenosine receptor agonists modulate glutamate release by activating inhibitory A 1 and excitatory A 2A receptors present on glutamatergic terminals of the rat cerebral cortex. British Journal of Pharmacology (2002) 136, 434–440; doi:10.1038/sj.bjp.0704712
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Adenosine, particularly through A1 receptor activation, inhibits release of neurotransmitters involved in central excitability and neural network regulation, including norepinephrine, acetylcholine, dopamine, and glutamate.
“Adenosine, particularly through A1 receptor activation, inhibits the release of neurotransmitters involved in central excitability and neural network regulation, including norepinephrine [32], acetylcholine [33,34], dopamine [35], and glutamate [36].”
From Pre-Exercise Caffeine as a Modulator of Exercise-Induced Acute Cardiometabolic Responses: A Narrative Review (2026) · cites this paper as [34]
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- Authors
- Marchi, M., Raiteri, L., Risso, F., Vallarino, A., Bonfanti, A., Monopoli, A., Ongini, E., & Raiteri, M.
- Affiliations
- University of Genoa (IT)
- Corresponding author
- Marchi, Mario
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2002-06
- Volume
- 136
- Issue
- 3
- Pages
- 434-440
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- OpenAlex
- W3087885511
- Cited by
- 96
- References
- 38
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 6 · 2023: 5 · 2022: 5 · 2021: 4 · 2020: 4 · 2019: 1 · 2018: 7 · 2017: 2 · 2016: 4 · 2014: 1 · 2013: 1 · 2012: 4
- FWCI
- 4.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Keywords
- adenosine A1 receptor, adenosine A2A receptor, glutamate release, synaptosomes, cerebral cortex, adenosine, DPCPX, SCH58261, CGS 21680, California Consumer Privacy Act, D-aspartate, glutamatergic terminals, adenosine receptor antagonists
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