Increase in blood-brain barrier permeability does not directly induce neuronal death but may accelerate ischemic neuronal damage

It is observed that the increase in blood-brain barrier (BBB) permeability (BBBP) is associated with ischemic stroke and thought to trigger neuronal damage and deteriorate ischemic infarction, even though there is no experimental proof. Here, we investigated the effect of BBBP increase on brain dama...

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Bibliographic Details
Published in:Experimental Animals 2018, Vol.67(4), pp.479-486
Main Authors: Ohmori, Chiemi, Sakai, Yusuke, Matano, Yasuki, Suzuki, Yasuhiro, Umemura, Kazuo, Nagai, Nobuo
Format: Article
Language:English
Subjects:
Acceleration
Apoptosis
Blood-brain barrier
Brain damage
Brain injury
Carotid artery
Cell death
Cerebral blood flow
Cerebral infarction
Infarction
Ischemia
ischemic stroke
Membrane permeability
Mice
Mortality
neuronal death
Occlusion
Original
Permeability
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Summary:It is observed that the increase in blood-brain barrier (BBB) permeability (BBBP) is associated with ischemic stroke and thought to trigger neuronal damage and deteriorate ischemic infarction, even though there is no experimental proof. Here, we investigated the effect of BBBP increase on brain damage, using a combination of photochemically-induced thrombotic brain damage (PIT-BD) model, a focal brain ischemic model, and transient bilateral carotid artery occlusion model (CAO, a whole brain ischemic model), in mice. In PIT-BD, BBBP increased in the region surrounding the ischemic damage from 4 h till 24 h with a peak at 8 h. On day 4, the damaged did not expand to the region with BBBP increase in mice with PIT-BD alone or with 30 min CAO at 1 h before PIT-BD, but expanded in mice with 30 min CAO at 3.5 h after PIT-BD. This expansion was paralleled with the increase in the number of apoptotic cells. These findings indicate that increase in BBBP does not cause direct neuronal death, but it facilitates ischemic neuronal loss, which was attributed, at least partially, to acceleration of apoptotic cell death.
ISSN:1341-1357
1881-7122
DOI:10.1538/expanim.18-0038