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Fig. 4. K_ATP channels delay a progressive anoxic Ca_i rise due to Ca²⁺ influx in whole-cell-recorded Purkinje neurons of cerebellar slices from juvenile mice. (A) CN^– (1 mmol l^–1) blocks spontaneous spiking due to a hyperpolarisation and concomitant increase in membrane conductance as measured in response to regular injection of hyperpolarising dc current pulses (see insets). During this phase of chemical anoxia, Ca_i shows a stable increase by <50 nmol l^–1. Several minutes after the onset of a spontaneous repolarisation of membrane potential in the presence of CN^–, a secondary progressive rise of Ca_i starts to develop. (B) The anoxic hyperpolarisation is caused by a prominent tolbutamide-sensitive outward current. In the presence of tolbutamide, the onset of the secondary progressive phase of the anoxic Ca_i rise develops almost immediately at the beginning of a CN^–-induced inward current that is usually masked by the K_ATP outward current. Holding potential: –60 mV. (C) In a Purkinje neuron, filled via the patch-electrode with 100 mmol l^–1 Cs⁺ and 30 mmol l^–1 TEA⁺ to block K⁺ currents, CN^– evokes an inward current accompanied by a major rise of Ca_i. These responses are not notably affected by bath application of 20 µmol l^–1 CNQX and 100 µmol l^–1 APV to block ionotropic glutamate receptors. (D) In a Cs⁺/TEA⁺ filled cell, the CN^–-induced Ca_i rise is abolished by Ca²⁺-free superfusate that also contains 5 mmol l^–1 Mg²⁺ to block Ca²⁺ channels and 1 mmol l^–1 EGTA to buffer extracellular Ca²⁺. All recordings from K. Ballanyi, M. Lückermann and D. W. Richter.

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