Reduced locomotion in the serum and glucocorticoid inducible kinase 3 knock out mouse

Undine E. Lang, David P. Wolfer, Florian Grahammer, Nathalie Strutz-Seebohm, Guiscard Seebohm, Hans Peter Lipp, James (Jim) McCormick, Rainer Hellweg, Kevin Dawson, Jian Wang, David Pearce, Florian Lang

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The serum and glucocorticoid inducible kinase isoform SGK3 is expressed in the brain including hippocampal neurons. It is activated by phosphoinositide-3 (PI3) kinase and thus a putative target of neurotrophic factors. In vitro experiments pointed to the ability of SGK3 to regulate several transporters and ion channels including the AMPA receptor GluR1. In order to explore the in vivo functional significance of SGK3 in the regulation of spatial learning and exploratory behavior, we assessed the performance of SGK3 knockout mice (SGK3-/-) and their wild type littermates (SGK3+/+) in a place navigation task in the water-maze, radial maze in a battery of forced and free exploration tests, acoustic startle and a test for motoric coordination. According to water-maze and radial maze testing reference and working memory was intact in SGK3-/- mice. However, detailed analysis of swimming patterns of SGK3-/- mice in the water-maze revealed a deficit in precision and goal-directed navigation in space. SGK3-/- mice showed reduced exploratory activity, which was observed in several environments and increased centre field avoidance in the open-field. SGK3-/- mice further showed reduced darting behavior on open surfaces, indicating that the knock out may modify basic patterns of locomotion. In conclusion, lack of SGK3 leads to subtle behavioral defects which may result from deranged neuronal regulation of transporters and ion channels.

Original languageEnglish (US)
Pages (from-to)75-86
Number of pages12
JournalBehavioural Brain Research
Volume167
Issue number1
DOIs
StatePublished - Feb 15 2006
Externally publishedYes

Fingerprint

Locomotion
Knockout Mice
Glucocorticoids
Ion Channels
Water
Spatial Behavior
Exploratory Behavior
Aptitude
1-Phosphatidylinositol 4-Kinase
AMPA Receptors
Nerve Growth Factors
Short-Term Memory
Acoustics
Protein Isoforms
Neurons
serum-inducible kinase
Brain

Keywords

  • AMPA receptors
  • Anxiety
  • Behavior
  • Depression
  • Memory

ASJC Scopus subject areas

  • Behavioral Neuroscience

Cite this

Lang, U. E., Wolfer, D. P., Grahammer, F., Strutz-Seebohm, N., Seebohm, G., Lipp, H. P., ... Lang, F. (2006). Reduced locomotion in the serum and glucocorticoid inducible kinase 3 knock out mouse. Behavioural Brain Research, 167(1), 75-86. https://doi.org/10.1016/j.bbr.2005.08.017

Reduced locomotion in the serum and glucocorticoid inducible kinase 3 knock out mouse. / Lang, Undine E.; Wolfer, David P.; Grahammer, Florian; Strutz-Seebohm, Nathalie; Seebohm, Guiscard; Lipp, Hans Peter; McCormick, James (Jim); Hellweg, Rainer; Dawson, Kevin; Wang, Jian; Pearce, David; Lang, Florian.

In: Behavioural Brain Research, Vol. 167, No. 1, 15.02.2006, p. 75-86.

Research output: Contribution to journalArticle

Lang, UE, Wolfer, DP, Grahammer, F, Strutz-Seebohm, N, Seebohm, G, Lipp, HP, McCormick, JJ, Hellweg, R, Dawson, K, Wang, J, Pearce, D & Lang, F 2006, 'Reduced locomotion in the serum and glucocorticoid inducible kinase 3 knock out mouse', Behavioural Brain Research, vol. 167, no. 1, pp. 75-86. https://doi.org/10.1016/j.bbr.2005.08.017
Lang UE, Wolfer DP, Grahammer F, Strutz-Seebohm N, Seebohm G, Lipp HP et al. Reduced locomotion in the serum and glucocorticoid inducible kinase 3 knock out mouse. Behavioural Brain Research. 2006 Feb 15;167(1):75-86. https://doi.org/10.1016/j.bbr.2005.08.017
Lang, Undine E. ; Wolfer, David P. ; Grahammer, Florian ; Strutz-Seebohm, Nathalie ; Seebohm, Guiscard ; Lipp, Hans Peter ; McCormick, James (Jim) ; Hellweg, Rainer ; Dawson, Kevin ; Wang, Jian ; Pearce, David ; Lang, Florian. / Reduced locomotion in the serum and glucocorticoid inducible kinase 3 knock out mouse. In: Behavioural Brain Research. 2006 ; Vol. 167, No. 1. pp. 75-86.
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