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Electrophysiological actions of hemoglobin on CA1 hippocampal neurons Ip, Joseph Ko Hung


Hemoglobin, the oxygen-carrying component of red blood cells, is known as a nitric oxide (NO) chelating agent. For this reason, hemoglobin has been used widely in studying the role of nitric oxide in long-term potentiation (LTP) and excitotoxicity. However, the direct electrophysiological actions of hemoglobin has not been examined. In this investigation, the actions of hemoglobin on rat hippocampal CAl neurons were studied since hemoglobin may be present in hemorrhagic stroke and other head injuries. Superfusion of rat hippocampal slices with 0.1 mM of bovine hemoglobin for 15 minutes was induced a significant depolarization associated with an increase in the input resistance. In addition, hemoglobin suppressed the evoked synaptic responses and increased the depolarization-induced discharge of action potentials, of rat hippocampal CAl neurons. These hemoglobin-mediated changes usually recovered partially 30 minutes after the removal of hemoglobin. While the depolarizing action of hemoglobin was enhanced in a calcium-free medium, it was not significantly changed by 2-amino-5-phosphonovalerate (APV) and 6- cyano-7-nitroquinoxaline-2,3-dione (CNQX). These observations suggest that the depolarizing action of hemoglobin is independent of the presence of extracellular calcium and activations of the excitatory amino acid receptors. Because hemoglobin has been observed to suppress the depolarizing action of glutamate, it is possible that hemoglobin suppresses the EPSP by interfering with the actions of glutamate. Although hemoglobin has been suggested to suppress LTP and excitability by scavenging nitric oxide (Garthwaite et al., 1988; Haley et al., 1992; 0’ Dell et al., 1991; Schuman and Madison, 1991), the reported actions of hemoglobin were not removed by pre-treatment with 100 pM or 500 pM of No-nitro-L-arginine, a nitric oxide synthase inhibitor. Similar to the scavenging property of hemoglobin, the iron content of hemoglobin probably did not contribute to the actions of hemoglobin since 0.4 mM or 2.0 mM of ferric chloride did not simulate the effects of hemoglobin. Because neurons can be exposed to hemoglobin in hemorrhagic stroke and head injuries, the electrophysiological actions of hemoglobin on rat hippocampal CAl neurons may be relevant to the neurological complications associated with intracranial hemorrhage and head injuries. Further studies on mechanisms of the electrophysiological actions of hemoglobin are necessary for understanding the role of hemoglobin in neuronal damages associated with hemorrhagic stroke and other head injuries.

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