Korean J Physiol Pharmacol.  2004 Apr;8(2):77-81.

Increase of Synapsin I, Phosphosynapsin (ser-9), and GAP-43 in the Rat Hippocampus after Middle Cerebral Artery Occlusion

• Jung YJ
• Huh PW
• Park SJ
• Park JS
• Lee KE

Abstract

The loss of neurons and synaptic contacts following cerebral ischemia may lead to a synaptic plastic modification, which may contribute to the functional recovery after a brain lesion. Using synapsin I and GAP-43 as markers, we investigated the neuronal cell death and the synaptic plastic modification in the rat hippocampus of a middle cerebral artery occlusion (MCAO) model. Cresyl violet staining revealed that neuronal cell damage occurred after 2 h of MCAO, which progressed during reperfusion for 2 weeks. The immunoreactivity of synapsin I and GAP-43 was increased in the stratum lucidum in the CA3 subfield as well as in the inner and outer molecular layers of dentate gyrus in the hippocampus at reperfusion for 2 weeks. The immunoreactivity of phosphosynapsin was increased in the stratum lucidum in the CA3 subfield during reperfusion for 1 week. Our data suggest that the increase in the synapsin I and GAP-43 immunoreactivity probably mediates either the functional adaptation of the neurons through reactive synaptogenesis from the pre-existing presynaptic nerve terminals or the structural remodeling of their axonal connections in the areas with ischemic loss of target cells. Furthermore, phosphosynapsin may play some role in the synaptic plastic adaptations before or during reactive synaptogenesis after the MCAO.

Keyword

Hippocampus; MCAO; Synapsin I; Phosphosynapsin; Growth associated protein-43 (GAP-43); Reactive synaptogenesis

MeSH Terms

Animals
Axons
Brain
Brain Ischemia
Cell Death
Dentate Gyrus
GAP-43 Protein*
Hippocampus*
Infarction, Middle Cerebral Artery*
Middle Cerebral Artery*
Neurons
Plastics
Rats*
Reperfusion
Synapsins*
Viola
GAP-43 Protein
Plastics
Synapsins