English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse
  1. View item / 
  2. Item Summary

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

Forebrain-specific trkB-receptor knockout mice: Behaviorally more hyperactive than "depressive"

MPS-Authors
/persons/resource/persons38867

Grunwald,  I. C.
Department: Molecular Neurobiology / Klein, MPI of Neurobiology, Max Planck Society;

/persons/resource/persons38927

Klein,  R.
Department: Molecular Neurobiology / Klein, MPI of Neurobiology, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Zörner, B., Wolfer, D., Brandis, D., Kretz, O., Zacher, C., Madani, R., et al. (2003). Forebrain-specific trkB-receptor knockout mice: Behaviorally more hyperactive than "depressive". Biological Psychiatry, 54(10), 972-982. doi:10.1016/s0006-3223(03)00418-9.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0012-22F5-4
Abstract
According to the neurotrophin hypothesis of depression, decreased activity of brain-derived neurotrophic factor (BDNF) contributes to behavioral and plasticity-related alterations in depressed patients. We investigated the hypothesis that mice with a forebrain-specific knockout of the trkB receptor, the main mediator of BDNF signaling, represent a genetic animal model for depression. METHODS: Using the CRE-loxP system, we bred trkB(CaMKII-CRE) mice with a trkB-receptor disruption in the forebrain. We subjected trkB-mutant mice to a battery of behavioral tests, comprising open field, elevated zero maze, emergence test, novel object test, and forced swim. Additionally, we investigated the hypothalamic-pituitary-adrenal (HPA) axis immunohistochemically and by plasma analyses. RESULTS: trkB(CaMKII-CRE) mice showed a stereotyped hyper-locomotion with reduced explorative activity, and impulsive reactions to novel stimuli. The trkB-mutant mice did not exhibit depressionlike behaviors such as increased "despair" in the forced swim test, increased anxiety in the elevated zero maze, or neophobia in the novel object test. Furthermore, no HPA dysregulation was observed under normal and stressful conditions. CONCLUSIONS: trkB(CaMKII-CRE) mice cannot be regarded as a genetic mouse model of depression. Instead, the behavioral symptoms of trkB(CaMKII-CRE) mice, comprising hyper-locomotion, stereotyped behaviors, and cognitive impairments, are similar to those postulated for mouse models of attention-deficit disorder.