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A recent report by Katayama and colleagues [doi 10.1038/mp.2008.97] shows that the the gene slitrk1 – a known risk factor for the developmental disorders Tourette’s syndrome and trichotillomania gives rise to increased levels of noradrenaline when the gene is inactivated in a developing mouse model. In the U. S., the most frequently prescribed medications for these disorders are clonidine hydrochloride (Catapres®) and guanfacine (Tenex®), which inhibit the synaptic transmission from presynaptic nerve terminals that express the alpha 2-adrenergic receptor. Thus, the mouse model (mice with the inactive slitrk1 gene were healthy but showed behavioral abnormalities that were normalized upon treatment with clonidine) seems to validate the current form of treatment since a reduction in noradrenergic release, might counteract the higher levels of noradrenaline associated with the risk-promoting slitrk1 mutation.
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