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The neural circuits regulating motivation and movement include midbrain dopaminergic neurons and associated inhibitory GABAergic and excitatory glutamatergic neurons in the anterior brainstem. Differentiation of specific subtypes of GABAergic and glutamatergic neurons in the mouse embryonic brainstem is controlled by a transcription factor  Tal1 . This study characterizes the behavioral and neurochemical changes caused by the absence of  Tal1  function. The  Tal1   cko   mutant mice are hyperactive, impulsive, hypersensitive to reward, have learning deficits and a habituation defect in a novel environment. Only minor changes in their dopaminergic system were detected. Amphetamine induced striatal dopamine release and amphetamine induced place preference were normal in  Tal1   cko   mice. Increased dopamine signaling failed to stimulate the locomotor activity of the  Tal1   cko   mice, but instead alleviated their hyperactivity. Altogether, the  Tal1   cko   mice recapitulate many features of the attention and hyperactivity disorders, suggesting a role for  Tal1  regulated developmental pathways and neural structures in the control of motivation and movement.

translational psychiatry

ADHD-like behaviors caused by inactivation of a transcription factor controlling the balance of inhibitory and excitatory neuron development in the mouse anterior brainstem