Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/4693
DC Field | Value | Language |
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dc.contributor.author | Cunha, Rodrigo A. | - |
dc.date.accessioned | 2008-09-01T14:12:51Z | - |
dc.date.available | 2008-09-01T14:12:51Z | - |
dc.date.issued | 2008 | en_US |
dc.identifier.citation | Neurochemistry International. 52:1-2 (2008) 65-72 | en_US |
dc.identifier.uri | https://hdl.handle.net/10316/4693 | - |
dc.description.abstract | Adenosine is a prototypical neuromodulator, which mainly controls excitatory transmission through the activation of widespread inhibitory A1 receptors and synaptically located A2A receptors. It was long thought that the predominant A1 receptor-meditated modulation by endogenous adenosine was a homeostatic process intrinsic to the synapse. New studies indicate that endogenous extracellular adenosine is originated as a consequence of the release of gliotransmitters, namely ATP, which sets a global inhibitory tonus in brain circuits rather than in a single synapse. Thus, this neuron-glia long-range communication can be viewed as a form of non-synaptic transmission (a concept introduced by Professor Sylvester Vizi), designed to reduce noise in a circuit. This neuron-glia-induced adenosine release is also responsible for exacerbating salient information through A1 receptor-mediated heterosynaptic depression, whereby the activation of a particular synapse recruits a neuron-glia network to generate extracellular adenosine that inhibits neighbouring non-tetanised synapses. In parallel, the local activation of facilitatory A2A receptors by adenosine, formed from ATP released only at high frequencies from neuronal vesicles, down-regulates A1 receptors and facilitates plasticity selectively in the tetanised synapse. Thus, upon high-frequency firing of a given pathway, the combined exacerbation of global A1 receptor-mediated inhibition in the circuit (heterosynaptic depression) with the local synaptic activation of A2A receptors in the activated synapse, cooperate to maximise salience between the activated and non-tetanised synapses. | en_US |
dc.description.uri | http://www.sciencedirect.com/science/article/B6T0B-4P37J9K-1/1/5bffd6691faba4edbd8db550a5bcb70d | en_US |
dc.format.mimetype | aplication/PDF | en |
dc.language.iso | eng | eng |
dc.rights | openAccess | eng |
dc.subject | Adenosine | en_US |
dc.subject | A1 receptor | en_US |
dc.subject | A2A receptor | en_US |
dc.subject | Nerve ending | en_US |
dc.subject | Nerve terminal | en_US |
dc.subject | Astrocyte | en_US |
dc.subject | Synaptic plasticity | en_US |
dc.subject | Modulation | en_US |
dc.title | Different cellular sources and different roles of adenosine: A1 receptor-mediated inhibition through astrocytic-driven volume transmission and synapse-restricted A2A receptor-mediated facilitation of plasticity | en_US |
dc.type | article | en_US |
dc.identifier.doi | 10.1016/j.neuint.2007.06.026 | - |
item.fulltext | Com Texto completo | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.grantfulltext | open | - |
item.languageiso639-1 | en | - |
item.openairetype | article | - |
item.cerifentitytype | Publications | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.orcid | 0000-0003-2550-6422 | - |
Appears in Collections: | FMUC Medicina - Artigos em Revistas Internacionais |
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filee3d89c7cd9a046c8bfb54185ac1e20e8.pdf | 387.8 kB | Adobe PDF | View/Open |
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