A mouse model for manic-and depressive-like behaviour

M Jukic, A Avin, O Mayseless, O Novikov, C Brodski

Research output: Chapter in Book/Report/Conference proceedingConference contribution


Genetic predisposition, dysfunction of monoaminergic neurons
and altered signaling pathways are each thought to play a
critical role in bipolar disorder. However, how these factors
interact in the pathophysiology and pharmacotherapy of this
disease is poorly understood. Previously, we demonstrated that
the mid-hindbrain organizer activates a genetic network
including Wnt1 and GSK3 that is essential in determining the
number of monoaminergic neurons generated in the brain
during development and present later in adulthood. Recently,
genes associated with the mid-hindbrain organizer have been
suggested as a susceptibility gene for a series of psychiatric
disorders. In preliminary studies, we discovered that mouse
mutants with an aberrant mid-hindbrain organizer show an
imbalance of monoaminergic neurotransmitters and model
behavioural and neuropathological aspects reminiscent of
bipolar disorder which could be reversed by acute and chronic
exposure to mood stabilizing drugs. We investigated manicand depressive-like behaviour in these mutants in order to test
the face validity of these mice as a model for bipolar disorder.
In addition, monoaminergic innervation and signal transduction pathways were studied in these mice, providing insights
into the neuropathological basis of the altered behaviour of the
mutants. In order to test the predictive validity of this animal
model, we investigated whether behavioural abnormalities in
the mutants can be reversed by acute and chronic exposure to
mood stabilizing drugs. Our findings will critically advance our
understanding of the genetic, developmental and neurobiological basis underlying manic- and depressive-like behaviour.
Original languageEnglish
Number of pages1
StatePublished - 2012


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