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Glucose/oxygen deprivation and reperfusion upregulate SNAREs and complexin in organotypic hippocampal slice cultures
Author(s) -
Park Su Jin,
Jung Yeon Joo,
Kim Yul A,
LeeKang Ji Hee,
Lee Kyung Eun
Publication year - 2008
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/j.1440-1789.2008.00927.x
Subject(s) - downregulation and upregulation , hippocampal formation , microbiology and biotechnology , chemistry , biology , neuroscience , biochemistry , gene
Brain ischemia activates Ca 2+ ‐dependent synaptic vesicle exocytosis. The synaptosomal‐associated protein 25 (SNAP‐25) and syntaxin proteins, located on presynaptic terminals, are components of the SNARE (soluble N ‐ethylmaleimide‐sensitive factor attachment protein receptor) complex and play a key role in regulating exocytosis. Changes in the expression of SNAREs could affect SNARE complex formation, fusion of vesicles with the presynaptic membrane, and release of neurotransmitters through exocytosis. To investigate the relationship of glucose/oxygen deprivation (GOD)/reperfusion‐induced neuronal damage and alteration of presynaptic function, we examined the expression of SNAREs and complexin during GOD and reperfusion using organotypic hippocampal slice cultures. Microtubule‐associated protein 2 (MAP‐2) staining and transmission electron microscopy showed that neuronal damage increased in a time‐dependent manner and both types of neuronal death can occur at different times during GOD and reperfusion. The immunoreactivity of SNAREs such as SNAP‐25, vesicle‐associated membrane protein and syntaxin and complexin increased in pyramidal cell bodies in the CA1 and CA3 areas in a time‐dependent manner following reperfusion. Our data suggest that alteration of presynaptic function may play a partial role in delayed neuronal death during GOD and reperfusion in organotypic hippocampal slice cultures.