Electrophysiological actions of hemoglobin on rat hippocampal CA1 pyramidal neurons.

Hemoglobin, the oxygen-carrying component of red blood cells, can be released from erythrocytes in hemorrhagic stroke and intracranial bleeding associated with head injuries. Therefore, neurons may be exposed to this agent. In addition, hemoglobin can chelate nitric oxide (NO) and has been used in studying the role of NO in synaptic plasticity and excitotoxicity. However, the electrophysiological actions of hemoglobin on central neurons are not well characterized. In the present investigation, the electrophysiological actions of hemoglobin on CA1 pyramidal neurons in rat hippocampal slices were studied with conventional intracellular pointed microelectrode- as well as perforated patch-recordings. Superfusion of rat hippocampal slices with hemoglobin (0.05 or 0.1 mM for 10-15 min) induced a depolarization of CA1 neurons and suppressed the stratum radiatum stimulation-induced excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). The hemoglobin-induced depolarization as well as the suppression of the synaptic transients were present in slices pretreated with 0.1 or 0.5 mM of N omega-nitro-L-arginine, a nitric oxide synthase inhibitor, suggesting that hemoglobin has electrophysiological actions on hippocampal CA1 neurons that are independent of its NO scavenging property.