FIGURE 1.

Effect of ethosuximide (ETX) on Na⁺ and K⁺ currents of rat thalamocortical (TC) and cortical neurons. (A1.) Whole cell currents elicited by a voltage ramp protocol (from -100 to 50 mV) in a TC neuron show the reversible reduction of the persistent Na⁺ current (I_NaP) by 750 μM ETX. A2, LTS, and associated action potential burst firing (top traces) produced by the current steps of increasing amplitude (bottom traces) from a membrane potential of -70 mV, in control conditions and in the presence of 1μM TTX. Note the smaller and delayed low threshold Ca²⁺ potential in the presence of 1 μM TTX for the two smallest current steps: this is due to the block by TTX of the non-inactivating Na⁺ current (I_NaP) underlying the LTS (see ref. 19 for details). Action potentials are truncated for clarity. (B1.) Steady-state current/voltage plot show the reversible reduction by 500μM ETX of the sustained outward whole cell current (left plot). In another TC neuron recorded in a low Ca²⁺ (0.5mM) – high Mg²⁺ (8mM) medium (right plot), 500μM ETX has no effect on the sustained current, indicating that its action is on the Ca²⁺–activated K current (I_k(ca)) component of the sustained outward current. (B2.) Two depolarizing current (0.3nA) pulses show an increased tonic firing in the presence of 500μM ETX.The plot on the right illustrates how this action is restricted to the smallest input currents (0.2–0.4nA). (C.) Whole cell currents elicited by a voltage ramp protocol (from −90 to 50mV) in a layer V cortical pyramidal neuron show the reduction of I_NaP by 750μM ETX. (D1.) Whole cell currents from another layer V pyramidal neuron show the reduction by 750μM ETX of outward K⁺ current(s). (D2.) This effect is abolished when ETX is applied in the presence of a low Ca²⁺ (0.5mM) – high Mg²⁺ (8mM) medium, indication that ETX is acting on I_k(ca). Panels A and B reproduced with permission from references 15 and 19; © 1998 by Society for Neuroscience.