Evidence map›Paper›PMID 23478133›Full record

ArticleThe Journal of physiology2013

Glucose sensitivity of mouse olfactory bulb neurons is conveyed by a voltage-gated potassium channel.

Kristal Tucker, Sukhee Cho, Nicolas Thiebaud, Michael X Henderson, Debra Ann Fadool

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Modulating the Excitability of Olfactory Output Neurons Affects Whole-Body Metabolism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  9. Article
  10. NIH Workshop Report: sensory nutrition and disease.The American journal of clinical nutrition · 2021
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Could the Olfactory System Be a Target for Homeopathic Remedies as Nanomedicines?Journal of alternative and complementary medicine (New York, N.Y.) · 2018
    Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Kristal TuckerFlorida State University, 319 Stadium Drive, 3008 King Life Sciences, Tallahassee, FL 32306, USA.
Sukhee Cho
Nicolas Thiebaud
Michael X Henderson
Debra Ann Fadool
Florida State University · US

Funding

Chemosensory Training Program (CTP)T32DC000044 · NIDCD · FLORIDA STATE UNIVERSITY · PI DEBRA Ann FADOOL · 1995 to 2026
$5.3M
Modulation of Olfactory Bulb Neuron Current PropertiesR01DC003387 · NIDCD · FLORIDA STATE UNIVERSITY · PI FADOOL, DEBRA ANN · 2003 to 2013
$2.7M
Glucose Sensitivity of Mitral Cell Neurons of the Olfactory BulbF31DC010097 · NIDCD · FLORIDA STATE UNIVERSITY · PI TUCKER, KRISTAL RAYLONE · 2009 to 2009
$32k
NIDCD NIH HHS F31 DC010097NIDCD NIH HHS R01 DC003387NIDCD NIH HHS T32 DC000044NIDCD NIH HHS T32 DC00044
6 · The paper itself

Abstract

The olfactory bulb has recently been proposed to serve as a metabolic sensor of internal chemistry, particularly that modified by metabolism. Because the voltage-dependent potassium channel Kv1.3 regulates a large proportion of the outward current in olfactory bulb neurons and gene-targeted deletion of the protein produces a phenotype of resistance to diet-induced obesity in mice, we hypothesized that this channel may play a role in translating energy availability into a metabolic signal. Here we explored the ability of extracellular glucose concentration to modify evoked excitability of the mitral neurons that principally regulate olfactory coding and processing of olfactory information. Using voltage-clamp electrophysiology of heterologously expressed Kv1.3 channels in HEK 293 cells, we found that Kv1.3 macroscopic currents responded to metabolically active (d-) rather than inactive (l-) glucose with a response profile that followed a bell-shaped curve. Olfactory bulb slices stimulated with varying glucose concentrations showed glucose-dependent mitral cell excitability as evaluated by current-clamp electrophysiology. While glucose could be either excitatory or inhibitory, the majority of the sampled neurons displayed a decreased firing frequency in response to elevated glucose concentration that was linked to increased latency to first spike and decreased action potential cluster length. Unlike modulation attributed to phosphorylation, glucose modulation of mitral cells was rapid, less than one minute, and was reversible within the time course of a patch recording. Moreover, we report that modulation targets properties of spike firing rather than action potential shape, involves synaptic activity of glutamate or GABA signalling circuits, and is dependent upon Kv1.3 expression. Given the rising incidence of metabolic disorders attributed to weight gain, changes in neuronal excitability in brain regions regulating sensory perception of food are of consequence.

Indexed as

AnimalsFemaleGlucoseHEK293 CellsHumansIn Vitro TechniquesKv1.3 Potassium ChannelMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsOlfactory BulbGlucoseKv1.3 Potassium Channel

Identifiers

PMID23478133
PMCPMC3678042
OpenAlexW2159141169

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.