Ionic requirements for bursting activity in lobster stomatogastric neurons

Summary The ionic requirements for bursting activity have been investigated in the electrically coupled PD-AB cells group of the Stomatogastric ganglion in the lobster.The passive electrical properties and coupling parameters have been determined in either current or voltage clamp conditions. In voltage clamped cells, the current displayed slow inward transients with superimposed fast transients corresponding respectively to the slow waves and spikes of the coupled undamped cells. The amplitude and frequency of the slow transients were reduced upon hyperpolarization.Cyclic conductance changes were observed with short current pulses, the coupling ratio also changes cyclically being lower during the bursts and slowly increasing during the interburst interval.The slow wave amplitude increased in low K-saline. The post-burst hyperpolarization but not the top level of the wave behaved like a potassium electrode for [K]_o higher than 10 mM/l.TEA at low concentration (1 to 5 mM/l) increased the slow wave amplitude by lifting its top level by 10 to 20 mV. The post-burst hyperpolarization remained almost unchanged and its K-dependence was not altered by TEA.Low Na-saline reduced the slow wave amplitude (6 to 11 mV per decade). The Na-dependence increased in the presence of TEA. Slow waves devoid of spikes persisted in 10% Na saline containing TEA. 10^–9 M/1 TTX blocked the spikes. 10^–7 M/1 TTX blocked the slow waves.Mg-free saline had no effect on the slow wave. In Ca-free saline the cells depolarized and the bursting activity tended to vanish. Repolarization with current led to long lasting slow waves deprived of post-burst hyperpolarization. The bursting ceased when EDTA was added to the Ca-free saline.Cobalt (up to 10 mM/l) was similar to Ca-free saline in its effects; lengthening of the wave and blockage of the repolarization. Replacing Ba for Ca produced large (up to 70 mV) slow waves which were reduced by Co and Ca.Bistable states were observed in various experimental conditions. It is concluded that the slow waves are produced by activation of sodium and calcium currents. The amplitude of the slow wave is modulated by the simultaneous activation of a TEA-sensitive K current. The repolarization is caused by increased K current activated by the inward calcium current. The slow pacemaker potential in the interburst interval corresponds to the slow disappearance of the K current.This work was supported by N.I.H. grant no. 09322, NSF grant no. 00250, and a Guggenheim Foundation Fellowship to A.D.S. and by the CNRS and a DGRST grant no. 16501891 to M. Gola. We are grateful to Stuart Thompson and Felix Strumwasser for helpful comments and to Barbara McLean for technical assistance.