Premium
Contributions of Ca 2+ and Zn 2+ to spreading depression‐like events and neuronal injury
Author(s) -
Dietz Robert M.,
Weiss John H.,
Shuttleworth C. William
Publication year - 2009
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2009.05853.x
Subject(s) - cortical spreading depression , depolarization , ischemia , cytosol , neuroscience , calcium , biophysics , ischemic injury , chemistry , medicine , biology , biochemistry , migraine , enzyme
The phenomenon of spreading depression (SD) involves waves of profound neuronal and glial depolarization that spread throughout brain tissue. Under many conditions, tissue recovers full function after SD has occurred, but SD‐like events are also associated with spread of injury following ischemia or trauma. Initial large cytosolic Ca 2+ increases accompany all forms of SD, but persistently elevated Ca 2+ loading is likely responsible for neuronal injury following SD in tissues where metabolic capacity is insufficient to restore ionic gradients. Ca 2+ channels are also involved in the propagation of SD, but the channel subtypes and cation fluxes differ significantly when SD is triggered by different types of stimuli. Ca 2+ influx via P/Q type channels is important for SD generated by localized application of high K + solutions. In contrast, SD‐like events recorded in in vitro ischemia models are not usually prevented by Ca 2+ removal, but under some conditions, Zn 2+ influx via L‐type channels contributes to SD initiation. This review addresses different roles of Ca 2+ in the initiation and consequences of SD, and discusses recent evidence that selective chelation of Zn 2+ can be sufficient to prevent SD under circumstances that may have relevance for ischemic injury.