Abstract
1. Oxygen and energy deficits induces a cascade of pathological processes which lead to neuronal dysfunction and cell death. 2. The pathogenesis of ischemia-induced neuronal damage includes a disturbed calcium homeostasis, an excessive release of EAA and an enhanced formation of free oxygen radicals. 3. Calcium antagonists inhibit Ca 2+ influx into the neuronal cell via VSCC. 4. Glutamate antagonists reduce intracellular Ca 2+ concentration by inactivation of NMDA receptor-associated calcium channels (NMDA antagonists) or AMPA/quisqualate receptor-linked sodium channels (non-NMDA antagonists). 5. Furthermore, oxygen radical scavengers can avoid neuronal damage. 6. Agonists of the adenosinergic and serotonergic transmitter systems contribute to neuroprotection by hyperpolarization of the neuronal membrane due to an increase of K + permeability
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