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The Olfactory Bulb: A Metabolic Sensor of Brain Insulin and Glucose Concentrations via a Voltage-Gated Potassium Channel

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Abstract

The voltage-gated potassium channel, Kv1.3, contributes a large proportion of the current in mitral cell neurons of the olfactory bulb where it assists to time the firing patterns of action potentials as spike clusters that are important for odorant detection. Gene-targeted deletion of the Kv1.3 channel, produces a “super-smeller” phenotype, whereby mice are additionally resistant to diet- and genetically-induced obesity. As assessed via an electrophysiological slice preparation of the olfactory bulb, Kv1.3 is modulated via energetically important molecules – such as insulin and glucose – contributing to the body’s metabolic response to fat intake. We discuss a biophysical characterization of modulated synaptic communication in the slice following acute glucose and insulin stimulation, chronic elevation of insulin in mice that are in a conscious state, and induction of diet-induced obesity. We have discovered that Kv1.3 contributes an unusual nonconducting role – the detection of metabolic state.

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Acknowledgments

We would like to thank Mr. Michael Henderson and Steven J. Godbey for routine technical assistance and mouse colony husbandry. We would like to thank Ms. Marita Madson for many insightful electrophysiological discussions. We would like to thank Mr. Charles Badland for artistic assistance in the visuals used in our oral presentation for this symposium. This work was supported by NIH grants R01 DC003387 & F31 DC010097 from the NIDCD, the Tallahassee Memorial Hospital/Robinson Foundation, and a Sabbatical Award from Florida State University.

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Correspondence to Debra Ann Fadool .

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Tucker, K. et al. (2011). The Olfactory Bulb: A Metabolic Sensor of Brain Insulin and Glucose Concentrations via a Voltage-Gated Potassium Channel. In: Meyerhof, W., Beisiegel, U., Joost, HG. (eds) Sensory and Metabolic Control of Energy Balance. Results and Problems in Cell Differentiation, vol 52. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-14426-4_12

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