http://www.cnr.it/ontology/cnr/individuo/prodotto/ID37866
Long-term exposure to the new nicotinic agonist 1,2-bis-cytisinylethane upregulates nicotinic receptor subtypes of SH-SY5Y human neuorblastoma cells. (Articolo in rivista)
- Type
- Label
- Long-term exposure to the new nicotinic agonist 1,2-bis-cytisinylethane upregulates nicotinic receptor subtypes of SH-SY5Y human neuorblastoma cells. (Articolo in rivista) (literal)
- Anno
- 2005-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1038/sj.bjp.0706434 (literal)
- Alternative label
Riganti L(1); Matteoni C(2); Di Angelantonio S(2); Nistri A(2); Gaimarri A(1); Sparatore F(3); Canu-Boido C(3); Clementi F(1); and Gotti C(1) (2005)
Long-term exposure to the new nicotinic agonist 1,2-bis-cytisinylethane upregulates nicotinic receptor subtypes of SH-SY5Y human neuorblastoma cells.
in British journal of pharmacology
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Riganti L(1); Matteoni C(2); Di Angelantonio S(2); Nistri A(2); Gaimarri A(1); Sparatore F(3); Canu-Boido C(3); Clementi F(1); and Gotti C(1) (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- 1. Inst Neurosci, CNR, Dept Med Pharmacol,Univ Milan, I-20129 Milan, Italy
2. SISSA, Sch Adv Int Studies, I-34014 Trieste, Italy
3. Univ Genoa, Dept Pharmaceut Sci, Genoa, Italy (literal)
- Titolo
- Long-term exposure to the new nicotinic agonist 1,2-bis-cytisinylethane upregulates nicotinic receptor subtypes of SH-SY5Y human neuorblastoma cells. (literal)
- Abstract
- Nicotinic drug treatment can affect the expression of neuronal nicotinic acetylcholine receptors ( nAChR) both in vivo and in vitro through molecular mechanisms not fully understood. The present study investigated the effect of the novel cytisine dimer 1,2-bisN-cytisinylethane (CC4) on nAChR natively expressed by SH-SY5Y neuroblastoma cells in culture.
2 CC4 lacked the agonist properties of cytisine and was a potent antagonist (IC50 220 nM) on nAChRs. Chronic treatment of SH-SY5Y cells with 1 mM CC4 for 48 h increased the expression of H-3-epibatidine (H-3-Epi; 3-4-fold) or I-125-alpha-bungarotoxin (I-125-alpha Bgtx; 1.2-fold) sensitive receptors present on the cell membrane and in the intracellular pool. Comparable data were obtained with nicotine or cytisine, but not with carbamylcholine, d-tubocurarine, di-hydro-beta-erythroidine or hexametonium.
3 Immunoprecipitation and immunopurification studies showed that the increase in H-3-Epi- binding receptors was due to the enhanced expression of alpha 3 beta 2 and alpha 3 beta 2 beta 4 subtypes without changes in subunit mRNA transcription or receptor half-life. The upregulation was not dependent on agonist/antagonist properties of the drugs, and did not concern muscarinic or serotonin receptors.
4 Whole-cell patch clamp analysis of CC4-treated cells demonstrated larger nicotine-evoked inward currents with augmented sensitivity to the blockers alpha-conotoxin MII or methyllycaconitine.
5 In conclusion, chronic treatment with CC4 increased the number of nAChRs containing beta 2 and alpha 7 subunits on the plasma membrane, where they were functionally active. In the case of beta 2-containing receptors, we propose that CC4, by binding to intracellular receptors, triggered a conformational reorganisation of intracellular subunits that stimulated preferential assembly and membrane-directed trafficking of beta 2-containing receptor subtypes (literal)
- Prodotto di
- Autore CNR
- Insieme di parole chiave
Incoming links:
- Autore CNR di
- Prodotto
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi
- Insieme di parole chiave di