期刊
NEURON
卷 58, 期 6, 页码 925-937出版社
CELL PRESS
DOI: 10.1016/j.neuron.2008.05.009
关键词
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资金
- NIGMS NIH HHS [R01 GM058234, R01 GM058234-09A1] Funding Source: Medline
- NIMH NIH HHS [R37 MH071739-04, R37 MH071739] Funding Source: Medline
- NINDS NIH HHS [R01 NS024067-24, R01 NS024067] Funding Source: Medline
Synaptic homeostasis, induced by chronic changes in neuronal activity, is well studied in cultured neurons, but not in more physiological networks where distinct synaptic circuits are preserved. We characterized inactivity-induced adaptations at three sets of excitatory synapses in tetrodotoxin-treated organo-typic hippocampal cultures. The adaptation to inactivity was strikingly synapse specific. Hippocampal throughput synapses (dentate-to-CA3 and CA3-to-CA1) were upregulated, conforming to homeostatic gain control in order to avoid extreme limits of neuronal firing. However, chronic inactivity decreased mEPSC frequency at CA3-to-CA3 synapses, which were isolated pharmacologically or surgically. This downregulation of recurrent synapses was opposite to that expected for conventional homeostasis, in apparent conflict with typical gain control. However, such changes contributed to an inactivity-induced shortening of reverberatory bursts generated by feedback excitation among CA3 pyramids, safeguarding the network from possible runaway excitation. Thus, synapse-specific adaptations of synaptic weight not only contributed to homeostatic gain control, but also dampened epileptogenic network activity.
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