Roles of GSK3β in odor habituation and spontaneous neural activity of the mouse olfactory bulb

PLoS One. 2013 May 3;8(5):e63598. doi: 10.1371/journal.pone.0063598. Print 2013.

Abstract

Glycogen synthase kinase 3β (GSK3β), a multifaceted kinase, is abundantly expressed in the brain, including the olfactory bulb (OB). In resting cells, GSK3β is constitutively active, and its over-activation is presumably involved in numerous brain diseases, such as Alzheimer's disease. However, the functions of the constitutively active GSK3β in the adult brain under physiological conditions are not well understood. Here, we studied the possible functions of GSK3β activity in the OB. Odor stimulation, or blockade of peripheral olfactory inputs caused by either transgenic knock-out or ZnSO4 irrigation to the olfactory epithelium, all affected the expression level of GSK3β in the OB. When GSK3β activity was reduced by a selective inhibitor, the spontaneous oscillatory activity was significantly decreased in the granule cell layer of the OB. Furthermore, local inhibition of GSK3β activity in the OB significantly impaired the odor habituation ability. These results suggest that GSK3β plays important roles in both spontaneous neural activity and odor information processing in the OB, deepening our understanding of the potential functions of the constitutively active GSK3β in the brain under physiological conditions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Enzyme Inhibitors / pharmacology
  • Gene Expression
  • Glycogen Synthase Kinase 3 / antagonists & inhibitors
  • Glycogen Synthase Kinase 3 / genetics
  • Glycogen Synthase Kinase 3 / metabolism*
  • Glycogen Synthase Kinase 3 beta
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Odorants*
  • Olfactory Bulb / cytology
  • Olfactory Bulb / drug effects
  • Olfactory Bulb / metabolism*
  • Olfactory Mucosa / cytology
  • Olfactory Mucosa / drug effects
  • Olfactory Mucosa / metabolism*
  • Olfactory Perception / physiology*
  • Smell / physiology*
  • Zinc Sulfate / pharmacology

Substances

  • Enzyme Inhibitors
  • Zinc Sulfate
  • Glycogen Synthase Kinase 3 beta
  • Gsk3b protein, mouse
  • Glycogen Synthase Kinase 3

Grants and funding

The work is supported by National Natural Science Foundation of China (91132307/H09, 31171061/C090208 and 20921004) to FX, Chinese Academy of Science (XDB02050500) to FX. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.