International Mammalian Genome Society

The 16th International Mouse Genome Conference (2002)


Oral Presentation

Wednesday 20 November

16:45 - 17:00 HRS

MOOD DISORDER IN MICE LACKING a1G T-type Ca2+ CHANNELS

H-S Shin
Korea Institute of Science and Technology

Co-Authors: 1) Kim D, 1) Park D, 2) Lee J-R, 1) Lee S, 2) Kim H-T
Institutions: 1) Korea Institute of Science and Technology, 2) Korea University

Mood disorders in humans can be grouped into two broad categories: major depression showing episodic depression only and bipolar disorder characterized by episodes of mania, with or without distinct episodes of depression (APA, 1993). No specific genetic mutations have been identified to cause these disorders. Here we present a mutant mouse that reveals the features of mood disorders. T-type Ca2+ channels control the firing pattern of thalamic neurons upon sensory inputs and have been implicated in the generation of sleep oscillation and absence seizures (Kim et al., Neuron 2001), but their role in waking status remains unknown. Although they were normal in home cage activities or in capacity for learning and memory in motor or spatial tasks, mice lacking a1G T-type Ca2+ channel revealed enhanced exploratory activities when put into novel environments. In an assay devised to measure the degree of playfulness upon encounter with novel objects, they showed active engagement with the objects as evidenced by shorter latency to the first contact, increased number of contacts and active displacement of the objects, when compared with control mice. They also showed resistance to depression as measured by the tail-suspension or forced swim test. These manic behaviors of the mutant were controllable by mood stabilizing drugs often used for human affective disorders. Sensorimotor gating was abnormal in the mutant as measured by pre-pulse inhibition of acoustic startle. These findings suggest that a1G T-type Ca2+ channels play a crucial role in the mood regulation and may point molecular mechanisms underlying mood disorders in humans.


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