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Title: PI-3 kinase and IP3 are both necessary and sufficient to mediate NT3-induced synaptic potentiation
Author: Yang, F ; He, XP ; Feng, LY ; Mizuno, K ; Liu, XW ; Russell, J ; Xiong, WC ; Lu, B
Source: NATURE NEUROSCIENCE
Issued Date: 2001
Volume: 4, Issue:1, Pages:19-28
Keyword: LONG-TERM POTENTIATION ; DEVELOPING NEUROMUSCULAR SYNAPSES ; NEUROTROPHIN SIGNAL-TRANSDUCTION ; NERVE GROWTH-FACTOR ; BDNF KNOCKOUT MICE ; PHOSPHATIDYLINOSITOL 3-KINASE ; HIPPOCAMPAL-NEURONS ; CORTICAL-NEURONS ; TRANSMISSION ; RECEPTOR
Subject: Neurosciences & Neurology
Corresponding Author: Lu, B (reprint author), NICHD, Unit Synapse Dev & Plast, Dev Neurobiol Lab, NIH, Bethesda, MD 20892 USA,
English 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 is blocked 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.
Indexed Type: sci
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/2082
Appears in Collections:神经所(总)_期刊论文

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Yang, F; He, XP; Feng, LY; Mizuno, K; Liu, XW; Russell, J; Xiong, WC; Lu, B.PI-3 kinase and IP3 are both necessary and sufficient to mediate NT3-induced synaptic potentiation,NATURE NEUROSCIENCE,2001,4(1):19-28
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