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This Article Full Text Full Text (PDF) All Versions of this Article: 579/3/691    most recent jphysiol.2006.126094v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Balfour, R. H. Articles by Trapp, S. Search for Related Content PubMed PubMed Citation Articles by Balfour, R. H. Articles by Trapp, S. Related Collections Cellular

¹ Department of Anaesthetics, Pain Medicine and Intensive Care, Chelsea & Westminster Hospital, Imperial College London, UK
² Biophysics Section, Blackett Laboratory, Imperial College London, UK

A proportion of dorsal vagal neurones (DVN) are glucosensors. These cells respond to brief hypoglycaemia either with a K_ATP channel-mediated hyperpolarization or with depolarization owing to an as yet unknown mechanism. K_ATP currents are observed not only during hypoglycaemia, but also in response to mitochondrial inhibition. Here we show that similarly to the observations for K_ATP currents, both hypoglycaemia and inhibition of mitochondrial function elicited a small inward current that persisted in TTX in DVN of rat brainstem slices. Removal of glucose from the bath solution induced this inward current within 50 ± 4 s in one subpopulation of DVN and in 279 ± 36 s in another subpopulation. No such subpopulations were observed for the response to mitochondrial inhibition. Biophysical analysis revealed that mitochondrial inhibition or hypoglycaemia inhibited an openly rectifying K⁺ conductance in 25% of DVN. In the remaining cells, either an increase in conductance, with a reversal potential between –58 and +10 mV, or a parallel inward shift of the holding current was observed. This current most probably resulted from inhibition of the Na⁺–K⁺-ATPase and/or the opening of an ion channel. Recordings with electrodes containing 145 mM instead of 5 mM Cl^– failed to shift the reversal potential of the inward current, indicating that a Cl^– channel was not involved. In summary, glucosensing and non-glucosensing DVN appear to use common electrical pathways to respond to mitochondrial inhibition and to hypoglycaemia. We suggest that differences in glucose metabolism rather than differences in the complement of ion channels distinguish these two cell types.

(Received 4 December 2006; accepted after revision 8 January 2007; first published online 11 January 2007)
Corresponding author S. Trapp: Biophysics Section, Blackett Laboratory, South Kensington Campus, Imperial College London, London SW7 2AZ, UK. Email: s.trapp{at}imperial.ac.uk

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