title: Ascorbic acid prevents blood-brain barrier disruption and sensory deficit caused by sustained compression of primary somatosensory cortex.
abstract: Transient compression of rat somatosensory cortex has been reported to affect cerebral microvasculature and sensory function simultaneously. However, the effects of long-term cortical compression remain unknown. Here, we investigated whether and to what extent sustained but moderate epidural compression of rat somatosensory cortex impairs somatic sensation and/or cortical microvasculature. Electrophysiological and behavioral tests revealed that sustained compression caused only short-term sensory deficit, particularly at 1 day after injury. Although the diameter of cortical microvessels was coincidentally reduced, no ischemic insult was observed. By measuring Evans Blue and immunoglobulin G extravasation, the blood-brain barrier (BBB) permeability was found to dramatically increase during 1 to 3 days, but this did not lead to brain edema. Furthermore, immunoblotting showed that the BBB component proteins occludin, claudin-5, type IV collagen, and glial fibrillary acidic protein were markedly upregulated in the injured cortex during 1 to 2 weeks when BBB regained integrity. Conversely, treatment of ascorbic acid prevented compression-induced BBB disruption and sensory impairment. Together, these data suggest that sustained compression of the somatosensory cortex compromises BBB integrity and somatic sensation only in the early period. Ascorbic acid may be used therapeutically to modulate cortical compression and/or BBB dysfunction.
authors.affiliation: Institute of Neuroscience, Tzu Chi University, Hualien, Taiwan.
authors.forename: Jia-Li
authors.initials: JL
authors.lastname: Lin
authors.forename: Yung-Hsin
authors.initials: YH
authors.lastname: Huang
authors.forename: Yi-Ching
authors.initials: YC
authors.lastname: Shen
authors.forename: Hsuan-Chi
authors.initials: HC
authors.lastname: Huang
authors.forename: Pei-Hsin
authors.initials: PH
authors.lastname: Liu
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D001812:Blood-Brain Barrier / Q000378:metabolism* / Q000473:pathology; D001927:Brain Diseases / Q000378:metabolism / Q000517:prevention & control*; D062507:Claudin-5; D024141:Collagen Type IV / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000378:metabolism; D062793:Occludin; D051381:Rats; D017207:Rats, Sprague-Dawley; D012678:Sensation Disorders / Q000378:metabolism / Q000517:prevention & control*; D013003:Somatosensory Cortex / Q000378:metabolism* / Q000473:pathology; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D000975:Antioxidants; D062507:Claudin-5; C491510:Cldn5 protein, rat; D024141:Collagen Type IV; D005904:Glial Fibrillary Acidic Protein; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D062793:Occludin; C568987:Ocln protein, rat; D001205:Ascorbic Acid