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Fig. 2. K_ATP channels in dorsal vagal neurons of juvenile rodents. (A) Superfusion of nitrogen-gassed hypoxic saline causes tissue anoxia in the dorsal vagal nucleus of medullary slices kept at 30°C. In dorsal vagal neurons of rats, such anoxia results in a sustained hyperpolarisation and concomitant suppression of tonic action potential discharge that are reversed by the sulfonylurea K_ATP channel blocker tolbutamide (200 µmol l^–1). Whole-cell recordings were done using patch-electrodes containing (in mmol l^–1) 140 K-gluconate, 1 MgCl₂, 0.5 CaCl₂, 1 NaCl, 10 Hepes, pH 7.4. The electrodes also contained Na₂ATP at different concentrations, in most cases 1 mmol l^–1. However, varying the ATP concentration between 0 and 20 mmol l^–1 did not affect the membrane response to anoxia (Müller et al., 2002). (B) The anoxic hyperpolarisation is due to opening of single K_ATP channels, as revealed in this example for chemical anoxia due to bath application of 1 mmol l^–1 cyanide (CN^–). The sharp deflections on the cell-attached current (I_m) trace during control, CN^– plus tolbutamide (200 µmol l^–1) and wash are caused by tonic spiking. Holding potential: 0 mV. (C) Current traces of the recording in B at higher time resolution. (D) In an inside-out patch from a mouse dorsal vagal neuron, K_ATP channel activity is abolished by addition of 20 µmol l^–1 ATP to the superfusate mimicking the intracellular solution. Holding potential: –50 mV. (E) Antisense RNA-polymerase chain reaction (aRNA-PCR) analysis of cytoplasm obtained during whole-cell recording reveals that three dorsal vagal neurons (DVN1–3) of rats coexpress mRNA for the inward-rectifying K⁺ (K_ir) channel isoform, K_ir6.2, and the sulfonylurea receptor (SUR) isoform, SUR1. Obviously, dorsal vagal neurons express the same type of K_ATP channels as pancreatic ß-cells innervated by a subpopulation of these neurons. A, reproduced from Ballanyi and Kulik (1998); B, C and E, reproduced from Karschin et al. (1998); D, data from K. Ballanyi and J. Brockhaus.

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