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Electrophysiological characterization of Na⁺ currents in acutely isolated human hippocampal dentate granule cells

G. Reckziegel *¹, H. Beck *, J. Schramm ², C. E. Elger * and B. W. Urban ¹

1. Properties of voltage-dependent Na⁺ currents were investigated in forty-two dentate granule cells (DGCs) acutely isolated from the resected hippocampus of twenty patients with therapy-refractory temporal lobe epilepsy (TLE) using the whole-cell patch-clamp technique.

2. Depolarizing voltage commands elicited large, rapidly activating and inactivating Na⁺ currents (140 pS µm^-2; 163 mM extracellular Na⁺) that were reduced in amplitude by lowering the Na⁺ gradient (43 mM extracellular Na⁺). At low temperatures (8-12 °C), the time course of Na⁺ currents slowed and could be well described by the model of Hodgkin & Huxley.

3. Na⁺ currents were reversibly blocked by tetrodotoxin (TTX) and saxitoxin (STX) with a half-maximal block of 4·7 and 2·6 nM, respectively. In order to reduce series resistance errors, the Na⁺ current was partially blocked by low toxin concentrations (10-15 nM) in the experiments described below. Under these conditions, Na⁺ currents showed a threshold of activation of about -50 mV, and the voltages of half-maximal activation and inactivation were -29 and -55 mV, respectively.

4. The time course of recovery from inactivation could be described with a double-exponential function (time constants, 3-20 and 60-200 ms). The rapid and slow time constants showed a distinct voltage dependence with maximal values around -55 and -80 mV, respectively. These properties contributed to a reduction of the Na⁺ currents during repetitive stimulation that was more pronounced with higher stimulation frequencies and also showed a dependence on the holding potential.

5. In summary, the most striking features of DGC Na⁺ currents were the large current density and the presence of a current component showing a slow recovery from inactivation. Our data provide a basis for comparison with properties of Na⁺ currents in animal models of epilepsy, and for the study of drug actions in therapy-refractory epilepsy.

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