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Titolo:
ACUTE REGULATION OF NOREPINEPHRINE TRANSPORT - I - PROTEIN-KINASE-C-LINKED MUSCARINIC RECEPTORS INFLUENCE TRANSPORT CAPACITY AND TRANSPORTER DENSITY IN SK-N-SH CELLS
Autore:
APPARSUNDARAM S; GALLI A; DEFELICE LJ; HARTZELL HC; BLAKELY RD;
Indirizzi:
VANDERBILT UNIV,SCH MED,DEPT PHARMACOL NASHVILLE TN 37232 VANDERBILT UNIV,SCH MED,DEPT PHARMACOL NASHVILLE TN 37232 VANDERBILT UNIV,SCH MED,CTR MOL NEUROSCI NASHVILLE TN 37232 EMORY UNIV,SCH MED,DEPT ANAT & CELL BIOL ATLANTA GA 30322
Titolo Testata:
The Journal of pharmacology and experimental therapeutics
fascicolo: 2, volume: 287, anno: 1998,
pagine: 733 - 743
SICI:
0022-3565(1998)287:2<733:ARONT->2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN NEUROBLASTOMA-CELLS; NEURO-BLASTOMA CELLS; CALMODULIN-DEPENDENT KINASES; HUMAN DOPAMINE TRANSPORTER; CA2+-DEPENDENT ENHANCEMENT; PHOSPHOINOSITIDE TURNOVER; NORADRENALINE REUPTAKE; POSSIBLE INVOLVEMENT; INTRACELLULAR CA2+; MEDIATED INCREASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
52
Recensione:
Indirizzi per estratti:
Citazione:
S. Apparsundaram et al., "ACUTE REGULATION OF NOREPINEPHRINE TRANSPORT - I - PROTEIN-KINASE-C-LINKED MUSCARINIC RECEPTORS INFLUENCE TRANSPORT CAPACITY AND TRANSPORTER DENSITY IN SK-N-SH CELLS", The Journal of pharmacology and experimental therapeutics, 287(2), 1998, pp. 733-743

Abstract

Using SK-N-SH cells, we observe that muscarinic acetylcholine receptor activation by methacholine (MCh) rapidly and selectively diminishes I-NE transport capacity (Vmax) with little or no change in norepinephrine (NE) K-m and without apparent effects on membrane potential monitored directly under current clamp. Over the same time frame, MCh exposure reduces the density of [H-3]nisoxetine binding sites (Bmax) in intact cells but not in total membrane fractions, consistent with a loss of transport capacity mediated by sequestration of transporters rather than changes in intrinsic transport activity or protein degradation. Similar changes in NE transport and [H-3]nisoxetine binding capacity are observed after phorbol ester (beta-PMA) treatment. Inhibition of PKCby antagonists and downregulation of PKC by chronic treatment with phorbol esters abolishes beta-PMA-mediated effects but produce only a partial blockade of MCh-induced effects. Neither muscarinic acetylcholine receptor nor PKC activation require extracellular Ca++ to diminish NET activity. In contrast, treatment of cells with the Ca++/ATPase antagonist, thapsigargin in Ca++-free medium, eliminates the staurosporine-insensitive component of MCh regulation. These findings were further corroborated by the ability of 2-bis(o-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl)ester application in Ca++-free medium to abolish NET regulation by MCh. Although they may contribute tobasal NET expression, we could not implicate CaMKII-, PKA- or nitric oxide-linked pathways in MCh regulation. Together, these findings I) provide evidence in support of G-protein coupled receptor-mediated regulation of catecholamine transport, 2) reveal intracellular Ca++-sensitive, PKC-dependent and -independent pathways that serve to regulate NET expression and 3) indicate that the diminished capacity for NE transport evident after mAChR and PKC activation involves a redistribution of NET protein.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 03:54:13