期刊
JOURNAL OF NEUROSCIENCE
卷 41, 期 22, 页码 4768-4781出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0005-21.2021
关键词
astrocytes; barrel cortex; IGF-I; long-term depression; long-term potentiation; sensory discrimination
资金
- Agencia Estatal de Investigacion Spain/Fondo Europeo de Desarrollo Regional [BFU2016-80802-P]
- European Union [Ministerio de Economia y Competitividad (MINECO)]
- National Institutes of Health/National Institute of Neurological Disorders and Stroke [R01-NS-097312, R01-DA-048822]
- Centro de Investigacion Biomedica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)
- MINECO [SAF2016-76462-C2-1-P]
- National Council of Science, Technology and Technological Innovation (CONCYTEC, Peru) through the National Fund for Scientific and Technological Development (FONDECYT, Peru)
- FundacAo de Amparo a Pesquisa do Estado de SAo Paulo (FAPESP) [2017/14742-0, 2019/033685]
This study demonstrates that IGF-I signaling induces long-term potentiation of brain synapses in mice by activating astrocytic IGF-I receptors, resulting in changes in synaptic plasticity and animal behavior. The research reveals a novel mechanism of how IGF-I impacts cortical inhibitory synaptic plasticity and animal behavior through astrocytes.
Insulin-like growth factor-I (IGF-I) signaling plays a key role in learning and memory processes. While the effects of IGF-I on neurons have been studied extensively, the involvement of astrocytes in IGF-I signaling and the consequences on synaptic plasticity and animal behavior remain unknown. We have found that IGF-I induces long-term potentiation (LTPIGFI) of the postsynaptic potentials that is caused by a long-term depression of inhibitory synaptic transmission in mice. We have demon-strated that this long-lasting decrease in the inhibitory synaptic transmission is evoked by astrocytic activation through its IGF-I receptors (IGF-IRs). We show that LTPIGFI not only increases the output of pyramidal neurons, but also favors the NMDAR-dependent LTP, resulting in the crucial information processing at the barrel cortex since specific deletion of IGF-IR in cortical astrocytes impairs the whisker discrimination task. Our work reveals a novel mechanism and functional conse-quences of IGF-I signaling on cortical inhibitory synaptic plasticity and animal behavior, revealing that astrocytes are key ele-ments in these processes.
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