Altered dopaminergic neurotransmission has also been implicated as one of the mechanisms of hyperactivity disorders, including attention-deficit hyperactivity disorder (ADHD) 2. Extensive research has shown the roles of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and in the ventral tegmental area (VTA) in these behaviors 1, 2. 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.īrain functions behind movement, motivated behavior, attention, impulse control, and learning are regulated by neurons in the anterior brainstem. Increased dopamine signaling failed to stimulate the locomotor activity of the Tal1 cko mice, but instead alleviated their hyperactivity. Amphetamine induced striatal dopamine release and amphetamine induced place preference were normal in Tal1 cko mice. Only minor changes in their dopaminergic system were detected. The Tal1 cko mutant mice are hyperactive, impulsive, hypersensitive to reward, have learning deficits and a habituation defect in a novel environment.
This study characterizes the behavioral and neurochemical changes caused by the absence of Tal1 function.
Differentiation of specific subtypes of GABAergic and glutamatergic neurons in the mouse embryonic brainstem is controlled by a transcription factor Tal1.
The neural circuits regulating motivation and movement include midbrain dopaminergic neurons and associated inhibitory GABAergic and excitatory glutamatergic neurons in the anterior brainstem.
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