Prior visual experience increases children's use of effective haptic exploration strategies in audio-tactile sound-shape correspondences.

Sound-shape correspondence refers to the preferential mapping of information across the senses, such as associating a nonsense word like bouba with rounded abstract shapes and kiki with spiky abstract shapes. Here we focused on audio-tactile (AT) sound-shape correspondences between nonsense words and abstract shapes that are felt but not seen. Despite previous research indicating a role for visual experience in establishing AT associations, it remains unclear how visual experience facilitates AT correspondences. Here we investigated one hypothesis: seeing the abstract shapes improve haptic exploration by (a) increasing effective haptic strategies and/or (b) decreasing ineffective haptic strategies. We analyzed five haptic strategies in video-recordings of 6- to 8-year-old children obtained in a previous study. We found the dominant strategy used to explore shapes differed based on visual experience. Effective strategies, which provide information about shape, were dominant in participants with prior visual experience, whereas ineffective strategies, which do not provide information about shape, were dominant in participants without prior visual experience. With prior visual experience, poking-an effective and efficient strategy-was dominant, whereas without prior visual experience, uncategorizable and ineffective strategies were dominant. These findings suggest that prior visual experience of abstract shapes in 6- to 8-year-olds can increase the effectiveness and efficiency of haptic exploration, potentially explaining why prior visual experience can increase the strength of AT sound-shape correspondences.

A Pitx3-deficient developmental mouse model for fine motor, olfactory, and gastrointestinal symptoms of Parkinson's disease.

Parkinson's disease (PD) is characterized by the selective death of substantia nigra pars compacta (SNpc) dopaminergic neurons and includes both motor and non-motor symptoms. While numerous models exist for the study of typical PD motor deficits, fewer exist for non-motor symptoms. Previous studies have shown that a Pitx3-/- mouse model (aphakia or ak mouse) has specific developmental failure of the dopaminergic neuron population in the SNpc and that it can be used for the study of PD-related gross motor dysfunction as well as cognitive functional deficits. It remains unclear whether the aphakia mouse, both male and female, might also be used to model fine motor deficits and for additional studies of non-motor deficits associated with PD. Here, using an extensive battery of behavioral tests, we demonstrate that the aphakia mouse shows both gross and fine motor functional deficits compared with control mice. Furthermore, aphakia mice show deficits of olfactory function in buried pellet, odor discrimination and odor habituation/dishabituation tests. We also found that aphakia mice suffer from gastrointestinal dysfunction (e.g., longer whole gut transit time and colon motility deficits), suggesting that the mutation also affects function of the gut-brain axis in this animal model. Moreover, our data demonstrate that in the aphakia mouse, L-DOPA, the gold standard PD medication, can rescue both gross and fine motor function deficits but neither olfactory nor gastrointestinal symptoms, a pattern much like that seen in PD patients. Altogether, this suggests that the aphakia mouse is a suitable model for fine motor, olfactory and gastrointestinal behavioral studies of PD as well as for the development of novel disease-modifying therapeutics. SIGNIFICANCE STATEMENT: While several animal models are available to study the major motor symptoms of PD, there are fewer that replicate non-motor symptoms, which constitute a major source of morbidity for patients. Moreover, available models often require manipulations resulting in sudden massive cell loss and inflammation, both of which may interfere with understanding of the direct effects of dopaminergic neuronal loss in the SNpc. We describe a model of congenital SNpc cell deficiency in a Pitx3-/- mouse and characterize it with a battery of behavioral tests suggesting that it closely mimics non-motor as well as motor symptoms of PD, providing a useful insight into the effects of the nigrostriatal dopamine deficit. Taken together, these data suggest that the ak mouse represents a useful model to study dopaminergic system function for both motor and non-motor symptoms of PD.