IGF-I Governs Cortical Inhibitory Synaptic Plasticity By Astrocyte Activation
Noriega-Prieto, J. A.; Maglio, L. E.; Zegarra-Valdivia, J.; Pignatelli, J.; Fernandez, A. M.; Martinez-Rachadell, L.; Fernandes, J.; Nunez, A.; Araque, A.; Torres-Aleman, I.; Fernandez de Sevilla, D.
Show abstract
Insulin-like growth factor-I (IGF-I) signaling plays key regulatory roles in multiple processes of brain physiology and pathology. While the direct effects of IGF-I in neurons have been extensively studied, the astrocyte involvement in IGF-I signaling and the consequences on synaptic plasticity and animal behavior remain unknown. Here we show that IGF-I induces the long-term depression (LTD) of inhibitory synaptic transmission in the mouse barrel cortex. This LTD requires the activation of the IGF-I receptor (IGF-IR) in astrocytes, which stimulates astrocyte Ca2+ signaling and the release of ATP/adenosine that in turn activates A2A adenosine receptors at presynaptic inhibitory terminals. Specific deletion of IGF-IR in cortical astrocytes (IGF-IR-/-) impaired the behavioral performance in a whisker discrimination task. These results show novel mechanisms and functional consequences of IGF-I signaling on cortical inhibitory synaptic plasticity and animal behavior, revealing astrocytes as key elements in these processes.
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