Differential expression of synaptosome-associated protein 25 kDa [SNAP-25] in hippocampi of neonatal mice following exposure to human influenza virus in utero

被引:39
作者
Fatemi, SH
Sidwell, R
Kist, D
Akhter, P
Meltzer, HY
Bailey, K
Thuras, P
Sedgwick, J
机构
[1] Univ Minnesota, Sch Med, Dept Cell Biol & Neuroanat, Minneapolis, MN 55455 USA
[2] Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA
[3] Utah State Univ, Sch Vet Med, Inst Antiviral Res, Logan, UT 84322 USA
[4] Vanderbilt Univ, Dept Psychiat, Div Psychopharmacol, Nashville, TN USA
[5] Univ Minnesota, Sch Med, BIPL Lab, Minneapolis, MN 55455 USA
关键词
human influenza virus; second trimester of pregnancy; mice; hippocampus; SNAP-25; schizophrenia; autism;
D O I
10.1016/S0006-8993(98)00450-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We investigated the role of maternal exposure to human influenza virus [HI] in C57BL/6 mice on day 9 of pregnancy on the hippocampal expression of SNAP-25 in postnatal day 0 neonates, and compared them to sham-infected pups. The expression of SNAP-25 in infected neonates varied along the septotemporal axis of hippocampus and in various anatomic layers. Quantitative densitometric analysis of specific immunogold silver-enhanced SNAP-25 immunoreactivity [IR] showed increases of 40-347% over control in all septal-dorsal hippocampal layers except for the subplate layer. In mid septo-temporal hippocampus, SNAP-25 IR increased by 10-114% over control in all layers, except for the hippocampal plate, but the extent of this increase was smaller than in the dorsal-septal area. Finally, in temporal-ventral levels, SNAP-25 expression was reduced in all infected layers by 21-33% below control except for mild increases of 8.8 and 10% in subplate and hippocampal plate layers. Additionally, the infected SNAP-25 maximal density bin shifted to lower values dorsally and to higher values medially, with ventral maximal bins remaining unchanged when compared to controls. The differential expression of SNAP-25 in the hippocampi of infected neonates indicates a variable degree of vulnerability across the septo-temporal axis of hippocampus. It is surmised that while viral infection may induce excitotoxicity in the ventral hippocampus, it may cause reactive synapto-genesis in the medial and dorsal sectors of the developing brains of postnatal day 0 neonates. (C) 1998 Elsevier Science B.V. All rights reserved.
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页码:1 / 9
页数:9
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