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Routes of Zn 2+ entry in ischemia
Author(s) -
Weiss J. H.
Publication year - 2003
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 - 10.1046/j.1471-4159.85.s2.10_3.x
Subject(s) - nmda receptor , postsynaptic potential , biophysics , hippocampal formation , chemistry , divalent , neuroscience , excitatory postsynaptic potential , biology , biochemistry , receptor , organic chemistry
Synaptic release of Zn 2+ and its translocation into postsynaptic hippocampal pyramidal neurons may contribute to their degeneration in epilepsy or ischemia. Culture studies have revealed that of the three major routes of divalent cation entry [NMDA channels, voltage sensitive Ca 2+ channels (VSCC) and Ca‐A/K channels], Ca‐A/K channels exhibit the highest permeability to exogenously applied Zn 2+ . Until recently, there has been little information about routes through which synaptically released Zn 2+ enters postsynaptic neurons. In a recent study employing mouse hippocampal slice preparations subjected to brief oxygen and glucose deprivation (OGD), we found a Ca‐A/K channel antagonist, but not combined NMDA and VSCC antagonism, to attenuate both Zn 2+ accumulation in CA3 and CA1 pyramidal neurons and their subsequent injury. While overall Zn 2+ accumulation appears to reflect a combination of translocation and release from intracellular stores, present results suggest that Zn 2+ influx through Ca‐A/K channels may play a critical role in Zn 2+ dependent ischemic injury.