SUMMARY1. Using the whole-cell recording mode of the patch-clamp technique, we have investigated kinetic and selectivity properties of a low-voltage-activated (l.v.a.) Ca2+ current in chick and rat dorsal root ganglion (d.r.g.) neurones.2. L.v.a currents were activated at about -50 mV and reached maximum amplitudes between -30 and -20 mV with averages of -0-16 nA in chick and -03 nA in rat d.r.g. cells with 5 mM-extracellular Ca2+. Between -60 and -20 mV, the time to peak, tp, of this current decreased with increasing membrane depolarizations. An e-fold change of tp required a 14 mV potential change in chick and a 17 mV change in rat d.r.g. cells at 22 'C.3. Between -50 and + 20 mV inactivation of this current was fast, single exponential and voltage dependent. In rat, the time constant of inactivation, Th, was smaller and less voltage dependent than in chick.4. The amplitude of these currents increased by a factor of 5-10, when the extracellular Ca2+ concentration was changed from 1 to 95 mm. Amplitudes and kinetic parameters of the currents showed typical shifts along the voltage axis. No correlation between Ca2+ current amplitudes and activation-inactivation kinetics was found, suggesting that the reaction rates which control these processes are not dependent on Ca2+ entry. Recovery from inactivation was voltage dependent and developed with a timeconstant, Tr' in the order of 1 s. Tr was nearly halved by changing the potential from -80 to -120 mV.6. Tail currents associated with membrane repolarization were also voltage dependent and developed exponentially. Their time constant decreased by a factor of 3 when the potential was changed from -60 to -100 mV.7. A second and more prominent Ca2+ current was activated at potentials positive to -20 mV h.v.a.), masking the time course of l.v.a. currents. Between -20 and 0 mV, time to peak of the entire current increased by a factor of 2 but decreased again at higher membrane potentials. Inactivation also became significantly slower in this potential range.8. The contribution of the h.v.a. component to the total membrane current was

Hippocampal inhibitory postsynaptic potentials are depolarizing in granule cells but hyperpolarizing in CA3 neurons because the reversal potentials and membrane potentials of these cells differ. Here the hippocampal slice preparation was used to investigate the role of chloride transport in these inhibitory responses. In both cell types, increasing the intracellular chloride concentration by injection shifted the reversal potential of these responses in a positive direction, and blocking the outward transport of chloride with furosemide slowed their recovery from the injection. In addition, hyperpolarizing and depolarizing inhibitory responses and the hyperpolarizing and depolarizing responses to the inhibitory neurotransmitter gamma-aminobutyric acid decreased in the presence of furosemide. These effects of furosemide suggest that the internal chloride activity of an individual hippocampal neuron is regulated by two transport processes, one that accumulates chloride and one that extrudes chloride.

SUMMARY1. An intracellular voltage clamp in conjunction with a patch pipette utilizing feed-back to monitor local current from the soma membrane were used to analyse transient and stationary currents in bursting pacemaker neurones in Helix pomatia and H. levantina.2. A weak, net inward current flows during small (< 20 mV) depolarizations. This current exhibits slow activation kinetics, persistence during prolonged depolarization, and slow turning off at end of depolarization. Consequently, the steady-state current-voltage curve exhibits a region of negative resistance from about -55 to -35 mV.3. The slow inward current and the negative resistance characteristic are rapidly and -completely abolished by substitution of C02+ or La3+ for Ca2+ and are partially blocked by the Ca-blocking drug D-600. Substitution of Tris or glucose for Na+ significantly reduces the inward current only after 15-20 min exposure, recovery being equally slow.4. The inward current and the negative resistance characteristic of the I-V curve are greatly enhanced by Ba2+ substitution for Ca2+. This is ascribed in part to Ba2+ carrying current through the slow inward current channels and in part to a suppression of the late K+ current by Ba2+.5. The inward current is also present in many non-bursting neurones but fails to appear as a net inward current due to short circuiting by a leakage current or by the delayed potassium current. In these cells the slow inward current contributes to inward going rectification. Replacement of Ca2+ with Ba2+ enhances the current so as to produce a net inward current during small depolarizations in these neurones.6. It is concluded that the slow inward current is carried primarily by * On leave of absence from the

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SUMMARY1. In dissociated and cultured 2-5-day-old chick dorsal root ganglion cells, a large transient inward current could be activated in response to a 'step' increase in [H+]..2. Using the single-electrode patch clamp technique in its whole-cell configuration, the proton-induced current was graded with [H+]. and relaxed in 1-2 s.3. The pH dependence of the current was sigmoid with activation occurring at around pH 7-0 (at [Ca2+]. = 1 mM) and a maximum at pH 6-0-5-5.4. Small increases of [H+]., which by themselves failed to activate a significant amount of current, inactivated the proton-induced current. The half-maximum of inactivation occurred at pH 7-11 at [Ca2+]. = 5 mm, but this changed to pH 7-32 at[Ca2+]0 = 1 mM.5. The proton-induced inward current reversed direction at the Na+ equilibrium potential and was suppressed in the absence of [Na+] 9. Measurement of the voltage-gated Ca2+ current using short (30-50 ms) depolarizing pulses to zero showed that the Ca2+ current (ICa) but not the fast Na+ current ('Na) was completely suppressed during the time course of activation of INa(H)*