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Additional resources for Inflammatory Cells and Mediators in CNS Diseases (New Horizons in Therapeutics , Vol 2)
Lauritzen, M. and Schilling, L. (1987). Change of cerebrovascular reactivity after cortical spreading depression in cats and rats. Brain Research, 411, 72–80. J. (1994). Involvement of calcitonin gene regulating peptide (CGRP) and nitric oxide (NO) in pial artery dilatation elicited by cortical spreading depression. Brain Research, 637, 204–210. , Baethamn, A. and Schilling, L. (1988). Mediators of blood brain barrier dysfunction and formation of vasogenic brain edema. J. Cereb. Blood Flow and Metabolism, 8, 621–634.
In the PNS there is rapid upregulation of ICAM-1 and to a lesser extent VCAM-1, while in the optic nerve the endothelium does not appear to respond in this way, even though the microglia are activated and proliferating and there is an astrocyte response. Wallerian degeneration poses intriguing questions as to how tissue degeneration can activate stromal cells in the absence of endothelial activation and leucocyte recruitment. Cytokines and the CNS Key mediators in the initiation of an acute inflammatory response are cytokines such as interleukin-1ß (IL-1ß) and tumour necrosis factor-alpha (TNF−α).
1990). Neurogenic control of the circulation during global ischemia. Stroke, 21, 168–171. , Nozaki, K. and Kraig. P. (1993). Neocortical spreading depression provokes expression of c-fos protein-like immunoreactivity within trigeminal nucleus caudalis via trigeminovascular mechanisms. Neuroscience, 13, 1167–1177. W. R. (1995). Clinical experience with excitatory amino acid antagonist drugs. Stroke, 26, 503–513. B. and Sturm, E. (1923). Conditions determining the transplantation of tissues in the brain.