期刊
JOURNAL OF NEUROSCIENCE
卷 31, 期 50, 页码 18211-18222出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4838-11.2011
关键词
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资金
- National Institutes of Health [NS 31718, DP1 OD003347, NICHD 5T32HD007466, NINDS NRSA F32NS068161-02]
- Intellectual and Developmental Disorders Research Center [NIH NICHHD P30 HD18655]
Neonatal seizures can lead to epilepsy and long-term cognitive deficits into adulthood. Using a rodent model of the most common form of human neonatal seizures, hypoxia-induced seizures (HS), we aimed to determine whether these seizures modify long-term potentiation (LTP) and silent NMDAR-only synapses in hippocampal CA1. At 48-72 h after HS, electrophysiology and immunofluorescent confocal microscopy revealed a significant decrease in the incidence of silent synapses, and an increase in AMPARs at the synapses. Coincident with this decrease in silent synapses, there was an attenuation of LTP elicited by either tetanic stimulation of Schaffer collaterals or a pairing protocol, and persistent attenuation of LTP in slices removed in later adulthood after P10 HS. Furthermore, postseizure treatment in vivo with the AMPAR antagonist 2,3-dihydroxy-6-nitro-7-sulfonyl-benzo[f] quinoxaline (NBQX) protected against the HS-induced depletion of silent synapses and preserved LTP. Thus, this study demonstrates a novel mechanism by which early life seizures could impair synaptic plasticity, suggesting a potential target for therapeutic strategies to prevent long-term cognitive deficits.
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