It is generally acknowledged that congenitally blind individuals develop superior sensory abilities in order to compensate for their lack of vision. Substantial research has been done on somatosensory and auditory sensory information processing of the blind. However, relatively little information is available about compensatory plasticity in the olfactory domain. Although previous studies indicate that blind individuals have superior olfactory abilities, no studies so far have investigated their sense of smell in relation to social and affective communication. The current study compares congenitally blind and normal sighted individuals in their ability to discriminate and identify emotions from body odours. A group of 14 congenitally blind and 14 age- and sex-matched sighted control subjects participated in the study. We compared participants' abilities to detect and identify by smelling sweat from donors who had been watching excerpts from emotional movies showing amusement, fear, disgust, or sexual arousal. Our results show that congenitally blind subjects outperformed sighted controls in identifying fear from male donors. In addition, there was a strong tendency that blind individuals were also better in detecting disgust. Our findings reveal that congenitally blind individuals are better at identifying ecologically important emotions and provide new insights into the mechanisms of social and affective communication in blindness.
The formation of olfactory maps in the olfactory bulb (OB) is crucial for the control of innate and learned mouse behaviors. Olfactory sensory neurons (OSNs) expressing a specific odorant receptor project axons into spatially conserved glomeruli within the OB and synapse onto mitral cell dendrites. Combinatorial expression of members of the Kirrel family of cell adhesion molecules has been proposed to regulate OSN axonal coalescence; however, loss-of-function experiments have yet to establish their requirement in this process. We examined projections of several OSN populations in mice that lacked either Kirrel2 alone, or both Kirrel2 and Kirrel3. Our results show that Kirrel2 and Kirrel3 are dispensable for the coalescence of MOR1-3-expressing OSN axons to the most dorsal region (DI) of the OB. In contrast, loss of Kirrel2 caused MOR174-9-and M72-expressing OSN axons, projecting to the DII region, to target ectopic glomeruli. Our loss-of-function approach demonstrates that Kirrel2 is required for axonal coalescence in subsets of OSNs that project axons to the DII region and reveals that Kirrel2/3independent mechanisms also control OSN axonal coalescence in certain regions of the OB.
The tongue display unit (TDU) is a sensory substitution device that translates visual images into electrotactile stimulation that is transmitted to the tongue and leads to new perceptual skills following training. Trained users, including blind individuals, become capable of orientation discrimination, motion detection, shape recognition and they can also successfully use the TDU to navigate in an environment, locate objects and avoid obstacles. Many studies and discussions have focused on the effects of training at the behavioural level, and assumed that the effects shown in training blindfolded sighted individuals are similar to those observed in blind people. In doing so, we argue that behavioural research on sensory substitution shows a functionalist bias. Functionalism claims that mental processes can be individuated by their characteristic inputs and outputs, and that the physical realization of a given function introduces no relevant difference, as long as the function is the same. We emphasize here why this assumption biases the interpretation of sensory substitution devices.
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