Molecular Mechanisms of Ischemic Brain DamageEdited by
- K. Kogure
- K.-A. Hossmann
- B.K. Siesjö
- F.A. Welsh
During the last few years, research into cerebral ischemia has been partly redirected. The most important change is the emphasis on mechanisms of ischemic damage, and particularly on its cellular and molecular aspects. This book focuses attention on this new, rapidly developing, and exciting area of research. The topics chosen are those in which development is now rapid. The starting point is the widely recognised but poorly understood phenomenon of selective neuronal vulnerability. In an attempt to explain this selectivity, as contrasted to necrotic destruction of glial cells and vascular endothelium as well, the book has been centered on the perturbed metabolism of excitatory transmitters, of calcium, and of pH and also on important target molecules such as proteins and lipids.
Progress in Brain Research
Published: January 1985
- List of contributers. Preface. Section I. Selective Neuronal Vulnerability. Post-ischemic resuscitation of the brain: selective vulnerability versus global resistance (K.-A. Hossmann). Role of vascular factors in regional ischemic injury (F. A. Welsh). Selective neuronal vulnerability: morphological and molecular characteristics (W. A. Pulsinelli). Selective vulnerability of the hippocampus to ischemia - reversible and irreversible types of ischemic damage (T. Kirino, A. Tamura and K. Sano). Microphysiology of selectively vulnerable neurons (R. Suzuki, T. Yamaguchi, Y. Inaba and H. G. Wagner). Neurochemical correlates to selective neuronal vulnerability (T. Wieloch). Section II. Cellular Ca2+ and H+ Homeostasis. Calcium entry blockers: autoradiographic mapping of their binding sites in rat brain (P. Supavilai, R. Cortes, J. M. Palacios and M. Karobath). A role for the mitochondrion in the protection of cells against calcium overload? (D. G. Nicholls). Regulation of calcium transport in rat hippocampal mitochondria during development and following denervation (M. Baudry and G. Lynch). Acid-base homeostasis in the brain: physiology, chemistry, and neurochemical pathology (B. K. Siesjo). Heterogeneous distribution of hydrogen and bicarbonate ions during complete brain ischemia (R. P. Kraig, W. A. Pulsinelli and F. Plum). Section III. Alterations in Protein and Lipid Metabolism. Calmodulin and protein phosphorylation: implications in brain ischemia (J. Chin, T. M. Buckholz and R. J. DeLorenzo). Mechanisms underlying the neuronal response to ischemic injury. Calcium-activated proteolysis of neurofilaments (W. W. Schlaepfer and U.-J. P. Zimmerman). Cerebral protein synthesis and ischemia (W. Bodsch, K. Takahashi, A. Barbier, B. Grosse Ophoff and K.-A. Hossmann). Changes in lipid metabolism in traumatized spinal cord (P. Demediuk, R. D. Saunders, N. R. Clendenon, E. D. Means, D. K. Anderson and L. A. Horrocks). Cellular and molecular effects of polyunsaturated fatty acids in brain ischemia and injury (P. H. Chan, R. A. Fishman, S. Longar, S. Chen and A. Yu). Free radical damage of the brain following ischemia (K. Kogure, H. Arai, K. Abe and M. Nakano). Subject index.