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Letters to the Editor

Olesen and Balder propose an hypothesis concerning Leao’s spreading depression in the hippocampus (1). In it they speculate that emotionally cathected experiences which can trigger transient global amnesia, may excite the hippocampus resulting in depolarization. This neuronal activity might then release glutamate which in turn might somehow trigger spreading depression culminating in a reversible amnesia. What might mediate such a process of neuronal cell depolarization? Corticotropin releasing factor (CRF) may be a candidate for this role given it’s key action in the stress response syndrome (2). Moreover, Aldenhoff and colleagues have shown that CRF can depolarize hippocampal neurons particularly those in CAI and CA3 regions, which are the areas known to be affected in hypoxia-ischemia and aging, respectively, and thus in memory-related processes (3). Supporting this hypothesis is the facct that glutamate is felt to be a mediator of hypoxic-ischemic inury (4). In addition, kainic acid, which is a structural analog of glutamate, causes hippocampal neurotoxicity in the CA3 region (5 ) . It is of interest that glucocorticoids, also produced in the stress response, can cause increased hippocampal neuronal vulnerability to metabolic insults due to their excitatory catabolic effects there, which may be glutamate-mediated (5 ) . Therefore, it may be hypothesized that a stressful experience may result in elevated CRF and glucocorticoid release, either or both of which might have hippocampal effects resulting in Leao’s spreading Address B. T. Truax. M.D. Department of Neurology SUNYAB School of Medicine Autonomic Function Laboratory Erie County Medical Center Buffalo, New York 14215 USA