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

S H Fatemi, Robert Sidwell, David Kist, Pervez Akhter, Herbert Y. Meltzer, Kevin Bailey, Paul Thuras, Jerry Sedgwick

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46 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1-9
Number of pages9
JournalBrain Research
Issue number1
StatePublished - Jul 27 1998

Bibliographical note

Funding Information:
We are grateful to NARSAD, The Minnesota Medical Foundation and The University of Minnesota, Department of Psychiatry Faculty Seed Grant for provision of funds to carry out this project. S.H. Fatemi is a NARSAD young investigator. R. Sidwell was supported by NIAID contract No. 1-AI65291. We are thankful to Susan Rasmussen, Daryl Olson, Dea Million and Melanie Julian for typing the manuscript.


  • Autism
  • Hippocampus
  • Human influenza virus
  • Mice
  • SNAP-25
  • Schizophrenia
  • Second trimester of pregnancy


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