Heilbronn, Regine

Peterschmitt, Yvan

Plauth, Alexander

Sieghart, Werner

Sperk, Günther

Weger, Stefan

Wisden, William

BMC Pharmacology

English

PubMed

Yvan Peterschmitt

Stefan Weger

Alexander Plauth

Regine Heilbronn

William Wisden

Günther Sperk

Werner Sieghart

Springer - Publisher Connector

BioMed Central
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BMC Pharmacology
Open AccessMeeting abstract
Establishing a new mouse model for investigating the function of 
amygdala neurons in anxiety
Yvan Peterschmitt1,2, Stefan Weger3, Alexander Plauth3, Regine Heilbronn3, 
William Wisden4, Günther Sperk1 and Werner Sieghart*2
Address: 1Institute of Pharmacology, Medical University of Innsbruck, 6020 Innsbruck, Austria, 2Center for Brain Research, Medical University of 
Vienna, 1090 Vienna, Austria, 3Institute of Virology, Charité Centrum, Medical University of Berlin, 12203 Berlin, Germany and 4Institute of 
Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK
Email: Werner Sieghart* - werner.sieghart@meduniwien.ac.at
* Corresponding author    
Benzodiazepine site agonists modulate the firing pattern
of neurons via GABAA receptors and by that influence the
activity of the network in which they participate and cause
appropriate changes in behaviour. Since the amygdala is
involved in regulating anxiety, it can be expected that
GABAA receptors located in this brain region contribute to
the anxiolytic effects of benzodiazepine site agonists. Here
we take advantage of an in vivo mouse model [1] in which
a Phe to Ile point mutation was introduced into the gene
coding for the GABAA receptor γ2 subunit. This γ2F77I
mutation, which was also flanked by loxP sites, affects
only the benzodiazepine binding site of the respective
receptors, and mice carrying this mutation no longer are
sensitive to certain benzodiazepine site agonists but are
otherwise normal. Here we aim to selectively replace the
"benzodiazepine insensitive" mutated γ2F77I subunit by
a GFP-labeled native one in the amygdala of γ2F77Ilox
mice by a stereotaxic injection of recombinant adeno-
associated viral (rAAV) vectors expressing Cre-recombi-
nase and GFP-labeled wild-type γ2 subunits. It has been
demonstrated previously that the replaced wild-type sub-
units combine with endogenous subunits to form com-
pletely assembled receptors with normal subcellular
distribution. Then only those amygdala neurons express-
ing the GFP-labeled wild-type γ2 subunits can be modu-
lated by a systemic application of these benzodiazepine
site agonists and any behavioural effects observed with
these drugs must have been generated via these neurons.
In this report we present a preliminary characterization of
the newly developed mouse model demonstrating the
correct expression of Cre-recombinase and GFP-labeled
wild-type γ2 subunits in amygdala neurons by immuno-
histochemical and in situ hybridization techniques.
Future experiments aim to characterize our model by
behavioural pharmacology in paradigms of anxiety.
Acknowledgements
Financial support by the NFN-project S10203-B13 of the Austrian Science 
Fund is gratefully acknowledged.
References
1. Wulff P, Goetz T, Leppä E, Linden AM, Renzi M, Swinny JD, Veko-
vischeva OY, Sieghart W, Somogyi P, Korpi ER, Farrant M, Wisden
W: From synapse to behavior: rapid modulation of defined
neuronal types with engineered GABAA receptors.  Nature
Neurosci 2007, 10:923-929.
from 14th Scientific Symposium of the Austrian Pharmacological Society (APHAR)
Innsbruck, Austria. 21–22 November 2008
Published: 5 November 2008
BMC Pharmacology 2008, 8(Suppl 1):A35 doi:10.1186/1471-2210-8-S1-A35
<supplement> <title> <p>14<sup>th </sup>Scientific Symposium of the Austrian Pharmacological Society (APHAR)</p> </title> <editor>Andrea Laslop and Thomas Griesbacher</editor> <note>Meeting abstracts – A single PDF containing all abstracts in this Supplement is available <a href="http://www.biomedcentral.com/content/files/pdf/1471-2210-8-S1-full.pdf">here</a>.</note> <url>http://www.biomedcentral.com/content/pdf/1471-2210-8-S1-info.pdf</url> </supplement>
This abstract is available from: http://www.biomedcentral.com/1471-2210/8/S1/A35
© 2008 Peterschmitt et al; licensee BioMed Central Ltd. 


Establishing a new mouse model for investigating the function of amygdala neurons in anxiety

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From synapse to behavior: rapid modulation of defined neuronal types with engineered GABAA receptors. Nature Neurosci

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Establishing a new mouse model for investigating the function of amygdala neurons in anxiety

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