D-cycloserine 24 and 48 hours after asphyxial cardiac arrest has no effect on hippocampal CA1 neuropathology.
D-cycloserine 24 and 48 hours after asphyxial cardiac arrest has no effect on hippocampal CA1 neuropathology.
复制标题
窒息心脏骤停后 24 小时和 48 小时 D-环丝氨酸对海马 CA1 神经病理学没有影响。
DOI：
10.1038/jcbfm.2014.135
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Drew,KellyL
中科院分区：
文献类型：
--
作者：
Combs,VélváM;Crispell,HeatherD;Drew,KellyL
Stimulation of N-methyl-D-aspartate receptors (NMDAR) contributes to regenerative neuroplasticity following the initial excitotoxic insult during cerebral ischemia. Stimulation of NMDAR with the partial NMDAR agonist D-cycloserine (DCS) improves outcome and restores hippocampal synaptic plasticity in models of closed head injury. We thus hypothesized that DCS would improve outcome following restoration of spontaneous circulation (ROSC) from cardiac arrest (CA). DCS (10 mg/kg, IP) was administered toSprague-Dawleyrats (male, 250–330 g; 63–84 days old) 24 and 48 hours after 6 or 8 minutes of asphyxial CA. Heart rate and blood pressure declined similarly in all groups. Animals showed neurological deficits after 6 and 8 minutes CA (P< 0.05, Tukey) and these deficits recovered more quickly after 6 minutes than after 8 minutes of CA. CA decreased the number of healthy neurons within CA1 with no difference between 6 and 8 minutes duration of CA (180.8 ± 27.6 (naïve,n =5) versus 46.3 ± 33.8 (all CA groups,n =27) neurons per mm CA1). DCS had no effect on neurological deficits or CA1 hippocampal cell counts (P> 0.05, Tukey).
