Changes of immunoreactivity for synaptophysin ('protein p38') following a transient cerebral ischemia in the rat striatum.
Brain Res
; 616(1-2): 320-4, 1993 Jul 09.
Article
in En
| MEDLINE
| ID: mdl-8102940
ABSTRACT
We assessed the chronological change of the expression of synaptophysin, an integral glycoprotein on the presynaptic vesicles, after a transient cerebral ischemic insult in the rat. The ischemic lesion was consistently localized in the dorsolateral part of the striatum, which was clearly visualized by a depletion of calcineurin immunostaining or increases of immunoreactivities for glial fibrillary acidic protein and tyrosine hydroxylase. Immunoreactivity for synaptophysin was transiently increased in the ischemic lesions from 3 to 7 days after cerebral ischemia. Thereafter, synaptophysin immunostaining in the damaged areas gradually decreased and finally almost disappeared one month after surgery. Because synaptophysin is located in the presynaptic vesicle, and thought to be involved in presynaptic functions such as vesicle-membrane fusion and release of neurotransmitters, present findings suggest that loss of the postsynaptic site after ischemic insult induces a transient increase of the presynaptic functions, followed by a decrease of functional presynaptic activity or trans-synaptic retrograde degeneration of axon terminals.
Search on Google
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Ischemic Attack, Transient
/
Synaptophysin
/
Corpus Striatum
Limits:
Animals
Language:
En
Journal:
Brain Res
Year:
1993
Document type:
Article
Affiliation country:
Japan