期刊
EUROPEAN JOURNAL OF NEUROSCIENCE
卷 24, 期 11, 页码 3008-3016出版社
WILEY
DOI: 10.1111/j.1460-9568.2006.05189.x
关键词
excitatory amino acids; imaging; metabotropic receptors; neuroprotection; perinatal brain injury; steroids
资金
- NIMH NIH HHS [R01 MH52716, R01 MH052716, K01 MH068347-01A1] Funding Source: Medline
- NINDS NIH HHS [R01 NS040338, R01 NS40338] Funding Source: Medline
Hypoxic/ischernic (HI) brain injury in newborn full-term and premature infants is a common and pervasive source of life time disabilities in cognitive and locomotor function. In the adult, HI induces glutamate release and excitotoxic cell death dependent on NMDA receptor activation. In animal models of the premature human infant, glutamate is also released following HI, but neurons are largely insensitive to NMDA or AMPA/kainic acid (KA) receptor-mediated damage. Using primary cultured hippocampal neurons we have determined that glutamate increases intracellular calcium much more than kainic acid. Moreover, glutamate induces cell death by activating Type I metabotropic glutamate receptors (mGluRs). Pretreatment of neurons with the gonadal steroid estradiol reduces the level of the Type I metabotropic glutamate receptors and completely prevents cell death, suggesting a novel therapeutic approach to excitotoxic brain damage in the neonate.
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