Publication: Thalidomide inhibition of vascular remodeling and inflammatory reactivity in the quinolinic acid-injected rat striatum
Issued Date
2009-10-06
Resource Type
ISSN
03064522
Other identifier(s)
2-s2.0-69249206617
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Neuroscience. Vol.163, No.2 (2009), 601-608
Suggested Citation
J. K. Ryu, N. Jantaratnotai, J. G. McLarnon Thalidomide inhibition of vascular remodeling and inflammatory reactivity in the quinolinic acid-injected rat striatum. Neuroscience. Vol.163, No.2 (2009), 601-608. doi:10.1016/j.neuroscience.2009.07.006 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/28300
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Thalidomide inhibition of vascular remodeling and inflammatory reactivity in the quinolinic acid-injected rat striatum
Author(s)
Other Contributor(s)
Abstract
Effects of thalidomide administration on vascular remodeling, gliosis and neuronal viability have been studied in excitotoxin-injected rat striatum. Intrastriatal injection of quinolinic acid (QUIN) caused time-dependent changes (durations of 6 h, 1 and 7 d post-injection) in vascular remodeling. QUIN excitotoxic insult was associated with increased numbers of vessels (laminin or collagen IV markers) demonstrating considerable abnormalities in morphology, including short fragments and vascular loops. Non-lesioned striatum, with injection of phosphate buffer solution (PBS) as a vehicle, showed no evidence for vascular remodeling. A maximal extent of vascular remodeling was measured at 1 d post-QUIN and was correlated with marked increases in microgliosis (ED1 marker) and astrogliosis (glial fibrillary acidic protein [GFAP] marker) relative to control PBS injection. Double staining of laminin with ED1 and GFAP demonstrated areas of close association of glial cells with blood vessels. Treatment of QUIN-injected animals with the anti-inflammatory compound, thalidomide significantly inhibited vascular remodeling (by 43%) and reduced microgliosis (by 33%) but was ineffective in modifying extents of astrogliosis. Intrastriatal QUIN injection was associated with a marked loss of striatal neurons relative to non-lesioned control with thalidomide treatment exhibiting a significant degree of neuroprotection (24% recovery) against QUIN-induced neurotoxicity. These results suggest close links between microglial-mediated inflammatory responses and vascular remodeling, with inflammatory reactivity associated with, and contributing to, neuronal damage in excitotoxically-lesioned striatum. © 2009 IBRO.