Book of Abstracts - Australian Centre for Economic Research on ...

3rd Cell Stress Society International Congress on
Stress Responses in Biology and Medicine and
2nd World Conference <strong>of</strong> Stress
synaptotagmin, a Ca 2+ -dependent synaptic vesicle protein, brain-derived neurotrophic factor (BDNF) and its
receptor tropomyosin-related kinase B (TrkB) play important roles in hippocampus-dependent learning and
memory behavior. However, whether chronic exercise can improve learning and memory by upregulating
these molecules remains unraveled. To answer this question, male BALB/c mice were used as the animal
model. After 4 weeks <strong>of</strong> treadmill exercise training, the ability <strong>of</strong> learning and memory was evaluated by onetrial
passive avoidance test (PA), an aversive learning task. Hippocampal synaptotagmin and TrkB protein
expressions were determined by Western blotting, and BDNF was measured by ELISA. Our results showed
that after chronic treadmill exercise, 1) the retention latency <strong>of</strong> PA was increased; 2) protein levels <strong>of</strong>
hippocampal TrkB and synaptotagmin were elevated; 3) TrkB or synaptotagmin protein expression was
positively correlated with PA per<strong>for</strong>mance. These data suggest that the upregulation <strong>of</strong> synaptotagmin and
TrkB may contribute to the chronic exercise-facilitated hippocampus-dependent cognitive function.
7A_05_P
(poster section A2, poster board #79, 24 th <strong>of</strong> August)
TOWARDS THE GENETIC DISSECTION OF ANXIETY
L. Czibere, M. Bunck, E. Frank, M. S. Keßler, M. Kohli, T. Bettecken, R. Landgraf
Max-Planck-Institute <strong>of</strong> Psychiatry, 80804 Kraepelinstr. 2-10, Munich, Germany,
e-mail: czibere@mpipsykl.mpg.de
To investigate the genetic background <strong>of</strong> anxiety-related and depression-like behaviour in mice, two lines,
selectively inbred <strong>for</strong> high (“HAB”) and low anxiety-related behaviour (“LAB”), starting out from outbred
CD1 mice. As mutations in the genome are assumed to make up <strong>for</strong> the majority <strong>of</strong> genetic differences, we
plan to pinpoint them with a linkage analysis approach. For this, the ‘Mouse Medium Density Linkage Panel’
by Illumina, was used to genotype 1449 single nucleotide polymorphisms (SNPs) in HAB and LAB mice, as
well as in F1 progeny (HABxLAB).
The animals tested were derived from generation 20 or higher, providing a solid basis <strong>for</strong> genetically
homogenous lines.
In a first analysis, out <strong>of</strong> the 1449 loci tested, <strong>for</strong> 225 autosomal loci HAB and LAB mice both displayed
homozygosity, but <strong>for</strong> different alleles. Cross-mated animals (F1, HABxLAB) were all heterozygous <strong>for</strong> these
loci.
Compared to an inter-strain analysis approach using two standard inbred mouse strains (e.g. BALB/c and
C57BL6), where animals do not only differ in their anxiety-related behaviour, our intra-strain analysis
considerably reduces the number <strong>of</strong> in<strong>for</strong>mative SNPs. There<strong>for</strong>e, in our mouse lines, the number <strong>of</strong>
in<strong>for</strong>mative false positive SNPs, relevant to the behavioural phenotype, will be much lower.
Interestingly, about 1/3 <strong>of</strong> the opposite homozygous SNPs are concentrated on only 5 chromosomes,
whereas two chromosomes contained just 3 and 6 <strong>of</strong> these SNPs.
Altogether, the Illumina Mouse Medium Density Linkage Panel seems to provide a sufficient number <strong>of</strong>
in<strong>for</strong>mative SNPs as to allow the identification <strong>of</strong> a linkage region, causative <strong>for</strong> the development <strong>of</strong> the
anxiety trait. We are planning to genotype a larger number <strong>of</strong> freely segregating F2 generation animals
(F1xF1). From this we expect being able to identify true candidate regions <strong>for</strong> anxiety-related behaviour.
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