Abstract
Effects of apamin on rat sympathetic neurones were investigated by means of intracellular and extracellular recording. Apamin (50 nM) significantly shortened the after-hyperpolarization (AH) following the spike evoked by current injection and slightly decreased its peak amplitude without affecting the time course of the spike. The AH following the synaptically-evoked spike was also blocked by apamin. This effect was dose- and time-dependent (ID50 estimated by extracellular recording approximately 15 nM, 20 min after application) and poorly reversible. Transmission of a single volley was not affected by 50 nM apamin. Though a long depolarizing current caused one or two spikes in the cell, greater repetitive firing was observed in the presence of apamin. Spontaneous repetitive firing, however, was not observed except for anodal-break spikes. Resting potential and input membrane resistance were essentially unchanged by apamin. The maximum rate of rise of the Ca spike was not decreased by 50 nM apamin but the duration of the spike was lengthened by 60%. The AH following the Ca spike was also blocked by apamin. These results suggest that apamin suppressed the slow AH without any inhibition of the Ca flux into the cell and is useful as a blocker of GK(Ca) in the rat sympathetic neurone.
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