A role for LYNX2 in anxiety-related behavior
Author
Tekinay, A.B.
Nong, Y.
Miwa J.M.
Lieberam I.
Ibanez-Tallon I.
Greengard P.
Heintz, N.
Date
2009Source Title
Proceedings of the National Academy of Sciences of the United States of America
Print ISSN
0027-8424
Volume
106
Issue
11
Pages
4477 - 4482
Language
English
Type
ArticleItem Usage Stats
177
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views
133
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downloads
Abstract
Anxiety disorders are the most prevalent mental disorders in developed societies. Although roles for the prefrontal cortex, amygdala, hippocampus and mediodorsal thalamus in anxiety disorders are well documented, molecular mechanisms contributing to the functions of these structures are poorly understood. Here we report that deletion of Lynx2, a mammalian prototoxin gene that is expressed at high levels in anxiety associated brain areas, results in elevated anxiety-like behaviors. We show that LYNX2 can bind to and modulate neuronal nicotinic receptors, and that loss of Lynx2 alters the actions of nicotine on glutamatergic signaling in the prefrontal cortex. Our data identify Lynx2 as an important component of the molecular mechanisms that control anxiety, and suggest that altered glutamatergic signaling in the prefrontal cortex of Lynx2 mutant mice contributes to increased anxiety-related behaviors.
Keywords
AnxietyLYNX2
Nicotinic
Prefrontal cortex
glutamic acid
lynx2 protein
nicotine
nicotinic receptor
protein
unclassified drug
amygdaloid nucleus
animal experiment
animal tissue
anxiety disorder
article
controlled study
disease association
gene
gene deletion
gene expression
gene function
gene loss
hippocampus
human
human cell
lynx2 gene
molecular mechanics
mouse
neurotransmission
nonhuman
prefrontal cortex
priority journal
protein localization
protein protein interaction
receptor binding
regulator gene
thalamus dorsomedial nucleus
Animals
Anxiety
Anxiety Disorders
Behavior, Animal
Glutamic Acid
Membrane Glycoproteins
Mice
Mice, Mutant Strains
Neuropeptides
Protein Binding
Receptors, Nicotinic
Synaptic Transmission
Mammalia
Mus
Permalink
http://hdl.handle.net/11693/22803Published Version (Please cite this version)
http://dx.doi.org/10.1073/pnas.0813109106Collections
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