Insulin-like growth factor I potentiates kainate receptors through a phosphatidylinositol 3-kinase dependent pathway

被引:28
作者
de la Vega, AG [1 ]
Buño, W [1 ]
Pons, S [1 ]
Garcia-Calderat, MS [1 ]
Garcia-Galloway, E [1 ]
Torres-Aleman, I [1 ]
机构
[1] CSIC, Inst Cajal, E-28002 Madrid, Spain
关键词
insulin-like growth factor I; ionotropic glutamate receptors; kainate receptors; phosphatidylinositol; 3-kinase; synaptic plasticity;
D O I
10.1097/00001756-200105080-00047
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neurotrophic factors modulate synaptic plasticity through mechanisms that include regulation of membrane ion channels and neurotransmitter receptors. Recently, it was shown that insulin-like growth factor I (IGF-I) induces depression of AMPA-mediated currents without affecting NMDA-receptor function in neurons. We now report that IGF-I markedly potentiates the kainate-preferring ionotropic glutamate receptor in young cerebellar granule neurons expressing functional kainate-, but not AMPA-mediated currents. Potentiation of kainate responses by IGF-I is blocked by wortmannin, a phosphatidylinositol 3-kinase (PI3K) inhibitor, indicating a role for this kinase in the effect of IGF-I. These results reinforce the notion that modulation of ionotropic glutamate receptors are involved in the regulatory actions of IGF-I on neuronal plasticity. NeuroReport 12:1293-1296 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:1293 / 1296
页数:4
相关论文
共 18 条
[1]   Insulin-like growth factor-I and central nervous system development [J].
Anlar, B ;
Sullivan, KA ;
Feldman, EL .
HORMONE AND METABOLIC RESEARCH, 1999, 31 (2-3) :120-125
[2]   IGF-1 modulates N and L calcium channels in a PI 3-kinase-dependent manner [J].
Blair, LAC ;
Marshall, J .
NEURON, 1997, 19 (02) :421-429
[3]  
Carro E, 2000, J NEUROSCI, V20, P2926
[4]   LONG-TERM DEPRESSION OF GLUTAMATE-INDUCED GAMMA-AMINOBUTYRIC-ACID RELEASE IN CEREBELLUM BY INSULIN-LIKE GROWTH FACTOR-I [J].
CASTROALAMANCOS, MA ;
TORRESALEMAN, I .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (15) :7386-7390
[5]   Phosphorylation and IGF-1-mediated dephosphorylation pathways control the activity and the pharmacological properties of skeletal muscle chloride channels [J].
De Luca, A ;
Pierno, S ;
Liantonio, A ;
Camerino, C ;
Camerino, DC .
BRITISH JOURNAL OF PHARMACOLOGY, 1998, 125 (03) :477-482
[6]  
DELAVEGA AG, 1998, SOC NEUR ABSTR, V24, P1784
[7]   Neurotrophin modulation of NMDA receptors in cultured murine and isolated rat neurons [J].
Jarvis, CR ;
Xiong, ZG ;
Plant, JR ;
Churchill, D ;
Lu, WY ;
MacVicar, BA ;
MacDonald, JF .
JOURNAL OF NEUROPHYSIOLOGY, 1997, 78 (05) :2363-2371
[8]   Translocation of a calcium-permeable cation channel induced by insulin-like growth factor-I [J].
Kanzaki, M ;
Zhang, YQ ;
Mashima, H ;
Li, L ;
Shibata, H ;
Kojima, I .
NATURE CELL BIOLOGY, 1999, 1 (03) :165-170
[9]   Glutamate receptors of the kainate type and synaptic transmission [J].
Lerma, J ;
Morales, M ;
Vicente, MA ;
Herreras, O .
TRENDS IN NEUROSCIENCES, 1997, 20 (01) :9-12
[10]   Regulation of AMPA receptor-mediated synaptic transmission by clathrin-dependent receptor internalization [J].
Man, HY ;
Lin, JW ;
Ju, WH ;
Ahmadian, G ;
Liu, LD ;
Becker, LE ;
Sheng, M ;
Wang, YT .
NEURON, 2000, 25 (03) :649-662