Intracerebroventricular application of S100B selectively impairs pial arteriolar dilating function in rats

Brain Research
Benjarat ChangyaleketFernando D Testai

Abstract

S100B is an astrocyte-derived protein that can act through the receptor for advanced glycation endproducts (RAGE) to mediate either "trophic" or "toxic" responses. Its levels increase in many neurological conditions with associated microvascular dysregulation, such as subarachnoid hemorrhage (SAH) and traumatic brain injury. The role of S100B in the pathogenesis of microvasculopathy has not been addressed. This study was designed to examine whether S100B alters pial arteriolar vasodilating function. Rats were randomized to receive (1) artificial cerebrospinal fluid (aCSF), (2) exogenous S100B, and (3) exogenous S100B+the decoy soluble RAGE (sRAGE). S100B was infused intracerebroventricularly (icv) using an osmotic pump and its levels in the CSF were adjusted to achieve a concentration similar to what we observed in SAH. After 48 h of continuous icv infusion, a cranial window/intravital microscopy was applied to animals for evaluation of pial arteriolar dilating responses to sciatic nerve stimulation (SNS), hypercapnia, and topical suffusion of vasodilators including acetylcholine (ACh), s-nitroso-N-acetyl penicillamine (SNAP), or adenosine (ADO). Pial arteriolar dilating responses were calculated as the percentage change of art...Continue Reading

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Citations

Jul 22, 2016·Reviews in the Neurosciences·Zhao Zhong Chong
Jul 20, 2017·Journal of Neuroinflammation·Benjarat ChangyaleketHaoliang Xu
Jul 18, 2018·International Journal of Molecular Sciences·Shafqat Rasul ChaudhrySajjad Muhammad

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