Mechanism of Postinhibitory Rebound in Molluscan Neurons

Postinhibitory rebound (PIR) is an intrinsic property of manyneurons but the underlying mechanism is not well understood.We studied PIR and its relationship to spike adaptation in B-cellsisolated from the buccal ganglia of Aplysia. These neurons exhibitPIR following inhibitory synaptic input and following directmembrane hyperpolarization. Hyperpolarizing and depolarizingvoltage clamp pulses from the resting potential evoke slow changesin membrane current that persist in the form of tail currentsfollowing the pulses. A subtraction method was used to isolateslow tail currents for study. Current-voltage measurements indicatethat slow outward tail currents following depolarizing pulsesresult from increases in membrane conductance, while inwardtail currents following hyperpolarizations to –50 and–60 mV result from conductance decreases. The reversalpotential of both outward and inward tail current is between–60 and –70 mV. Tail currents activated by pulsesmore positive than –60 mV are sensitive to the externalK⁺ concentration and blocked by injection of Cs⁺ and TEA. WhenCa²⁺ influx is prevented by bathing cells in Ca²⁺ free salineor by adding Co²⁺ or Ni²⁺, the tail currents are reduced buta significant fraction of the current is insensitive to thesetreatments. More negative conditioning pulses activate a secondcomponent of inward tail current that is weakly sensitive toK⁺ but more strongly effected by substitution of N-methyl glucamineor Li⁺ for external Na⁺. We conclude that both PIR and adaptationresult from slow changes in a voltage dependent, non-inactivatingK⁺ conductance that is active at voltages near the resting potentialand is not tightly coupled to Ca²⁺ influx. In addition, a secondinward current is activated by large hyperpolarizing pulsesthat results from an increase in Na⁺ and K⁺ conductance. Thissecond process is likely to contribute to PIR under particularcircumstances.