Biomedical Engineering Reference
In-Depth Information
whiskers and hair, in 11 cages, and observed the changes in whisker pattern after
mixing. In all 11 cages, wild-type mice regrew full sets of whiskers and facial hair
within 2-4 weeks, while in five of the cages,
Dvl1
/
mice lost all whiskers and
facial hair. The wild-type mice with whiskers were then returned to their home
cage with their original wild-type littermates. Within 2 weeks, the whiskers of
the returned mice were now trimmed. In addition, whiskerless
Dvl1
/
mutant
mice regrewwhiskers when returned to their home cage. Thus, the genotype of
the cagemate determined the whisker pattern, demonstrating that this is in fact a
social behavior, and
Dvl1
/
mice displayed defective social interaction. Since
barbering is often performed by dominant animals within a cage, a social dom-
inance tube test was performed, pairing one wild-type against one
Dvl1
/
mouse. In the majority of cases, the wild-type mouse won the tube test trial.
Thus, wild-type mice are more dominant than the mutant mice, consistent with
the hypothesis that the aberrant whisker-trimming behavior of the
Dvl1
-
deficient mice is related to low levels of social interaction.
Dvl1
-deficient mice also displayed less huddling contact during home-
cage sleeping and displayed deficits in nest-building. Wild-type 129SvEv
mice generally slept huddled together. If commercial nestlet wafers were
provided to the mice, they built fluffy, well-formed nests within 45 min.
In contrast,
Dvl1
-deficient mice tended to sleep in scattered, random pat-
terns and did not build full nests. In fact, mutant mice tended to sleep on
top of intact nestlet material. Taken together, the abnormal whisker-
trimming behavior, the lack of huddling during sleep, and the poor nest-
building displayed by
Dvl1
-deficient mice demonstrate an essential role
for
Dvl1
in normal home-cage social behavior.
Other tests that measure motor, sensory, balance, and learning functions
were normal in the
Dvl1
mutants, suggesting that the social deficits observed
in these mice were not due to generalized neurological dysfunction. The
only other test found to be abnormal in
Dvl1
knock-out mice was prepulse
inhibition (PPI) of startle. PPI is thought to measure sensorimotor gating, a
process where inhibitory neural pathways filter the multitude of stimuli that
bombard the senses at any time, allowing attention to be focused on one
stimulus. Sensorimotor gating has no known correlate in social behavior,
but as it measures filtering inhibitory pathways, it would not be unreasonable
to propose that the PPI and social interaction deficits are related. We rep-
licated these findings of abnormal social behavior, but the PPI abnormalities
were variable (Long et al., 2004). Thus,
Dvl1
mutant mice have specific de-
fects in social behavior by several different measures, and
Dvl1
is an entry
point to genetic pathways important for social interaction. Further studies
will be needed to determine the role of
Dvls
in sensorimotor gating.