Electrogenesis of the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia.

Abstract

The ionic mechanisms of the slow surface positive (P)-potential and the slow inhibitory postsynaptic potential (IPSP), an intracellularly recorded P-potential in sympathetic ganglia, were analysed by means of sucrose-gap, intracellular microelectrode techniques, and voltage clamp technique. Both the P-potential and the slow IPSP consist of two different potential components, namely the ouabain-sensitive and the ouabain-insensitive components. The ouabain-sensitive component was enhanced by a moderate conditioning hyperpolarization. This component was most reasonably explained as a potential change generated by an activation of the elctrogenic Na+ pump. The ouabaininsensitive potential component of the P-potential and the slow IPSP decreased in the amplitude and finally reversed its polarity by conditioning hyperpolarization. The reversal potential of ouabain-insensitive component of slow IPSP and slow inhibitory postsynaptic current (IPSO) was close to the Ex. The amplitude of ouabain-insensitive component of P-potential and slow IPSP was markedly decreased by an elevation of external K+ concentration. The reversal potential of ouabain-insensitive component shifted to a more positive potential level in high K+ Ringer's solution. On the other hand, it was augmented in K+-free Ringer's solution. A reduction of the membrane resistance was observed during the generation of the slow IPSP, when the membrane potential of ganglion cells was held at a membrane potential level more negative than -60 mV. The slow IPSC recorded by voltage-clamp method was associated with an increase in membrane conductance. It was concluded that the ouabain-insensitive component was generated by an activarion of K+ conductance.

A patch‐clamp study on the muscarine‐sensitive potassium channel in bullfrog sympathetic ganglion cells.

“…This mechanism found in cultured cells may underlie the K+ conductance-induced mechanism of the slow IPSP (Horn & Dodd, 1981;Dodd & Horn, 1983;Akasu & Koketsu, 1983) described in neurones of freshly isolated ganglia. The voltage-independent and muscarine-sensitive properties of the background K+ channel conform to a linear relationship between the amplitude of the slow IPSP and membrane potential (Dodd & Horn, 1983) and a linear current-voltage relationship for the synaptic current underlying slow IPSP (Akasu & Koketsu 1983). It has been believed until recently that the slow IPSP is generated only in C-type neurones in bullfrog sympathetic ganglia Dodd & Horn, 1983).…”

“…This idea is not consistent with the present finding that the muscarinicsensitive background K+ channel was observed in large-sized (40-70 ,um in diameter) neurones which could be B-type. Akasu & Koketsu (1983) have explicitly shown that the slow IPSP which is reversed in amplitude at -90 mV can be recorded intracellularly from B-type neurones in the nicotinized sympathetic ganglion. 243 244 K. KOYANO, K. TANAKA AND K. KUBA Therefore, the muscarine-facilitated K+ channel activities found in cultured bullfrog sympathetic ganglion cells are likely to account for the generation of the slow IPSP not only in C-type but also in B-type neurones in situ.…”

“…This idea is not consistent with the present finding that the muscarinicsensitive background K+ channel was observed in large-sized (40-70 ,um in diameter) neurones which could be B-type. Akasu & Koketsu (1983) have explicitly shown that the slow IPSP which is reversed in amplitude at -90 mV can be recorded intracellularly from B-type neurones in the nicotinized sympathetic ganglion.…”

“…The slow EPSP results from one or both of two actions mediated by the ml-subtype of the muscarinic receptor (mAChR; Tsuji & Kuba, 1988): (a) inhibition of a K+ current (Weight & Votava, 1970;Kuba & Koketsu, 1976) which is voltage dependent and non-inactivating (IM; Brown & Adams, 1980); and (b) activation of a voltage-independent and non-selective cation current (ID; Kuba & Koketsu, 1976;Akasu, Gallagher, Koketsu & ShinnickGallagher, 1984;Jones, 1985;Tsuji & Kuba, 1988). In contrast, the slow IPSP is produced by an increase in K+ conductance (Dodd & Horn, 1983) as well as by an activation of the electrogenic Na+ pump (Akasu & Koketsu, 1983). The singlechannel currents underlying the mAChR-induced slow IPSP have neither been recorded nor characterized in vertebrate neurones.…”

Analysis of a decreased Na+ conductance by tumor necrosis factor in identified neurons of Aplysia kurodai

“…Na' -pump (Oomura et al, 1974;Akasu et al, 1978;Akasu and Koketsu, 1983). We previously reported that in Aplysia inhibition of long duration (ILD) neurons, iontophoretically injected CAMP stimulates the Na+ -K + pump component of the ILD (Sawada et al, 1980).…”