http://www.cnr.it/ontology/cnr/individuo/prodotto/ID38072
Purinergic receptors mediate two distinct glutamate release pathways in hippocampal astrocytes (Articolo in rivista)
- Type
- Label
- Purinergic receptors mediate two distinct glutamate release pathways in hippocampal astrocytes (Articolo in rivista) (literal)
- Anno
- 2006-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1074/jbc.M510679200 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Fellin T.; Pozzan T.; Carmignoto G. (literal)
- Pagina inizio
- Pagina fine
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- Rivista
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- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Fellin T.; Pozzan T.; Carmignoto G.; Institute of Neurosciene CNR and University of Padova, Dipartimento Sci Biomed Sperimentali, Padova, Italy (literal)
- Titolo
- Purinergic receptors mediate two distinct glutamate release pathways in hippocampal astrocytes (literal)
- Abstract
- The purinergic P2X7 receptor (P2X7R) can mediate glutamate
release from cultured astrocytes. Using patch clamp recordings, we
investigated whether P2X7Rs have the same action in hippocampal
astrocytes in situ. We found that 2- and 3-O-(4-benzoylbenzoyl)
ATP (BzATP), a potent, although unselective P2X7R agonist,
triggers two different glutamate-mediated responses in CA1
pyramidal neurons; they are transient inward currents, which have
the kinetic and pharmacological properties of previously described
slow inward currents (SICs) due to Ca2?-dependent glutamate
release from astrocytes, and a sustained tonic current. Although
SICs were unaffected by P2X7Rs antagonists, the tonic current was
inhibited, was amplified in low extracellular Ca2?, and was insensitive
to glutamate transporter and hemichannel inhibitors. BzATP
triggered in astrocytes a large depolarization that was inhibited by
P2X7R antagonists and amplified in low Ca2?. In low Ca2? BzATP
also induced lucifer yellow uptake into a subpopulation of astrocytes
and CA3 neurons. Our results demonstrate that purinergic
receptors other than the P2X7R mediate glutamate release that
evokes SICs, whereas activation of a receptor that has features similar
to the P2X7R, mediates a sustained glutamate efflux that generates
a tonic current in CA1 neurons. This sustained glutamate
efflux, which is potentiated under non-physiological conditions,
may have important pathological actions in the brain (literal)
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