TY - CHAP
T1 - The olfactory bulb
T2 - A metabolic sensor of brain insulin and glucose concentrations via a voltage-gated potassium channel
AU - Tucker, Kristal
AU - Cavallin, Melissa Ann
AU - Jean-Baptiste, Patrick
AU - Biju, K. C.
AU - Overton, James Michael
AU - Pedarzani, Paola
AU - Fadool, Debra Ann
N1 - Funding Information:
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.
PY - 2010
Y1 - 2010
N2 - 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.
AB - 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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U2 - 10.1007/978-3-642-14426-4_12
DO - 10.1007/978-3-642-14426-4_12
M3 - Chapter
C2 - 20865378
AN - SCOPUS:77957739869
SN - 9783642144257
T3 - Results and Problems in Cell Differentiation
SP - 147
EP - 157
BT - Sensory and Metabolic Control of Energy Balance
A2 - Meyerhof, Wolfgang
A2 - Joost, Hans-Georg
A2 - Beisiegel, Ulrike
ER -
