Serotonin and dopamine are speculated to subserve motivationally opponent functions, but this hypothesis has not been directly tested. We studied the role of these neurotransmitters in probabilistic reversal learning in nearly 700 individuals as a function of two polymorphisms in the genes encoding the serotonin and dopamine transporters (SERT: 5HTTLPR plus rs25531; DAT1 3'UTR VNTR). A double dissociation was observed. The SERT polymorphism altered behavioral adaptation after losses, with increased lose-shift associated with L' homozygosity, while leaving unaffected perseveration after reversal. In contrast, the DAT1 genotype affected the influence of prior choices on perseveration, while leaving lose-shifting unaltered. A model of reinforcement learning captured the dose-dependent effect of DAT1 genotype, such that an increasing number of 9R-alleles resulted in a stronger reliance on previous experience and therefore reluctance to update learned associations. These data provide direct evidence for doubly dissociable effects of serotonin and dopamine systems.

The treatment of patients suffering from cerebral blindness following stroke is a topic of much recent interest. Several types of treatment are under investigation, such as substitution with prisms and compensation training of saccades. A third approach, aimed at vision restitution is controversial, as a proper controlled study design is missing. In the current study, 27 chronic stroke patients with homonymous visual field defects were trained at home with a visual training device. We used a discrimination task for two types of stimuli: a static point stimulus and a new optic flow-discontinuity stimulus. Using a randomized controlled crossover design, each patient received two successive training rounds, one with high contrast stimuli in their affected hemifield (test) and one round with low-contrast stimuli in their intact hemifield (control). Goldmann and Humphrey perimetry were performed at the start of the study and following each training round. In addition, reading performance was measured. Goldmann perimetry revealed a statistically significant reduction of the visual field defect after the test training, but not after the control training or after no intervention. For both training rounds combined, Humphrey perimetry revealed that the effect of a directed training (sensitivity change in trained hemifield) exceeded that of an undirected training (sensitivity change in untrained hemifield). The interaction between trained and tested hemifield was just above the threshold of significance (p = 0.058). Interestingly, reduction of the field defect assessed by Goldmann perimetry increases with the difference between defect size as measured by Humphrey and Goldmann perimetry prior to training. Moreover, improvement of visual sensitivity measured by Humphrey perimetry increases with the fraction of non-responsive elements (i.e., more relative field loss) in Humphrey perimetry prior to training. Reading speed revealed a significant improvement after training. Our findings demonstrate that our training can result in reduction of the visual field. Improved reading performance after defect training further supports the significance of our training for improvement in daily life activities.

White stimulus training-induced VFE can lead to improved color and shape perception and to increased reading speed in and beyond the pretraining transition zone if ECSG is sufficiently large. The latter depends on the eccentricity of the VFE.

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