Plasticity of neuron-glial interactions mediated by astrocytic EphARs

被引:53
作者
Nestor, Michael W.
Mok, Lee-Peng
Tulapurkar, Mohan E.
Thompson, Scott M.
机构
[1] Univ Maryland, Sch Med, Dept Physiol, Neurosci Program, Baltimore, MD 21201 USA
[2] Univ Maryland, Sch Med, Membrane Biol Training Program, Baltimore, MD 21201 USA
关键词
astrocyte; ephrin; Eph receptor; plasticity; hippocampus; electrophysiology;
D O I
10.1523/JNEUROSCI.2442-07.2007
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Ephrin (Eph) signaling via Eph receptors affects neuronal structure and function. We report here that exogenous ephrinAs (EphAs) induce outgrowth of filopodial processes from astrocytes within minutes in rat hippocampal slice cultures. Identical effects were induced by release of endogenous ephrinAs by cleavage of their glycosylphosphatidylinositol anchor. Reverse transcription-PCR and immunocytochemistry revealed the expression of multiple EphA receptors (EphARs) in astrocytes. Exogenous and endogenous ephrins did not induce process outgrowth from astrocytes transfected with a kinase-dead EphAR construct, indicating that the critical EphARs were located on glia. Concomitant with these morphological changes, ephrinA reduced the frequency of (S)-3,5- dihydroxyphenylglycine-evoked NMDA receptor-mediated inward currents in CA1 pyramidal cells, elicited by release of glutamate from glial cells. The sensitivity of CA1 cell synaptic or extrasynaptic NMDA receptors was unaffected by ephrinA, indicating that this effect was mediated by inhibition of glutamate release from glial cells. Finally, ephrinA application decreased the frequency and increased the duration of spontaneous oscillations of the intracellular [Ca2+] in astrocytes. We conclude that ephrinA-EphA signaling is a pluripotent regulator of neuron astrocyte interactions mediating rapid structural and functional plasticity.
引用
收藏
页码:12817 / 12828
页数:12
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