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Titolo:
PI-3 kinase and IP3 are both necessary and sufficient to mediate NT3-induced synaptic potentiation
Autore:
Yang, F; He, XP; Feng, LY; Mizuno, K; Liu, XW; Russell, J; Xiong, WC; Lu, B;
Indirizzi:
NICHD, Unit Synapse Dev & Plast, Dev Neurobiol Lab, NIH, Bethesda, MD 20892 USA NICHD Bethesda MD USA 20892 ev Neurobiol Lab, NIH, Bethesda, MD 20892 USA Inst Neurosci, Shanghai 200031, Peoples R China Inst Neurosci Shanghai Peoples R China 200031 ai 200031, Peoples R China NICHD, Sect Cell Biol & Signal Transduct, Lab Mol & Cellular Neurophysiol,NIH, Bethesda, MD 20892 USA NICHD Bethesda MD USA 20892 ular Neurophysiol,NIH, Bethesda, MD 20892 USA Univ Alabama, Dept Pathol, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 ept Pathol, Birmingham, AL 35294 USA
Titolo Testata:
NATURE NEUROSCIENCE
fascicolo: 1, volume: 4, anno: 2001,
pagine: 19 - 28
SICI:
1097-6256(200101)4:1<19:PKAIAB>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; DEVELOPING NEUROMUSCULAR SYNAPSES; NEUROTROPHIN SIGNAL-TRANSDUCTION; NERVE GROWTH-FACTOR; BDNF KNOCKOUT MICE; PHOSPHATIDYLINOSITOL 3-KINASE; HIPPOCAMPAL-NEURONS; CORTICAL-NEURONS; TRANSMISSION; RECEPTOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Lu, B NICHD, Unit Synapse Dev & Plast, Dev Neurobiol Lab, NIH, Bethesda, MD 20892 USA NICHD Bethesda MD USA 20892 robiol Lab, NIH, Bethesda, MD 20892 USA
Citazione:
F. Yang et al., "PI-3 kinase and IP3 are both necessary and sufficient to mediate NT3-induced synaptic potentiation", NAT NEUROSC, 4(1), 2001, pp. 19-28

Abstract

Signaling mechanisms underlying neurotrophic regulation of synaptic transmission are not fully understood. Here we show that neurotrophin-3 (NT3)-induced potentiation of synaptic transmission at the neuromuscular synapses isblocked by inhibition of phosphoinositide-3 kinase, phospholipase C-gamma or the downstream IP3 receptors of phospholipase C-gamma, but not by inhibition of MAP kinase. However, neither stimulation of Ca2+ release from intracellular stores by photolysis of caged IP3, nor expression of a constitutively active phosphoinositide-3 kinase (PI3K(star)) in presynaptic motoneurons alone is sufficient to enhance transmission. Photo-uncaging of IP3 in neurons expressing PI3K(star) elicits a marked synaptic potentiation, mimicking the NT3 effect. These results reveal an involvement of PI3 kinase in transmitter release, and suggest that concomitant activation of PI3 kinase and IP3 receptors is both necessary and sufficient to mediate the NTS-induced synaptic potentiation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 00:42:03