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The interaction may involve dopamine systems in the CNS.
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Reasons for the comorbidity are unknown, but may involve brain dopamine or insulin receptor activity.
Activity is an intriguing risk factor because in humans hyperactivity, often in the form of attention deficit hyperactivity disorder (ADHD), may involve dysregulation of dopamine signaling [28] and adult ADHD is associated with poor monitoring of child behavior [29].
Resistance to BRC therapy may involve defects in D2 dopamine receptor expression and possibly its posttranscriptional splicing [ 6, 7].
It might be that improved sustained attention is due to improved noradrenergic functioning following low doses and that the higher doses reducing overactivity and impulsiveness may involve other neuromodulators like dopamine in addition to norepinephrine.
Thus, the dynorphin/κ system mimics stressor administration in animals in producing aversive effects and inducing drug-seeking behavior, and this aversive response may involve reciprocal interactions with nucleus accumbens dopamine and the brain extrahypothalamic CRF system.
Given these earlier studies in the literature and the present findings, it is possible to speculate that risk for schizophrenia may involve the effects of rs1076560 on striatal dopamine signaling and its relationship with prefrontal activity.
This analysis revealed that the transcriptional effects of tianeptine may involve increased activity of noradrenaline, serotonin and dopamine neurotransmission.
Dopamine is considered to be a key player in reward-related behaviors [11] and because maternal neglect may involve a lack of reward from offspring, dysregulation of dopamine is a candidate mechanism for neglect.
Thus, the contextual reward influences on dopamine responses to unrewarded stimuli may involve pseudoconditioning or higher-order context conditioning.
Mechanistically this may involve increases in membrane permeant H2O2 which can oxidize dopamine within dopaminergic neurons to dopaminochrome which, via interaction with mitochondrial complex I, can result in increased mitochondrial superoxide.
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