title: From attentional gating in macaque primary visual cortex to dyslexia in humans.
abstract: Selective attention is an important aspect of brain function that we need in coping with the immense and constant barrage of sensory information. One model of attention (Feature Integration Theory) that suggests an early selection of spatial locations of objects via an attentional spotlight would also solve the 'binding problem' (that is how do different attributes of each object get correctly bound together?). Our experiments have demonstrated modulation of specific locations of interest at the level of the primary visual cortex both in visual discrimination and memory tasks, where the actual locations of the targets was also important in being able to perform the task. It is suggested that the feedback mediating the modulation arises from the posterior parietal cortex, which would also be consistent with its known role in attentional control. In primates, the magnocellular (M) and parvocellular (P) pathways are the two major streams of inputs from the retina, carrying distinctly different types of information and they remain fairly segregated in their projections to the primary visual cortex and further into the extra-striate regions. The P inputs go mainly into the ventral (temporal) stream, while the dorsal (parietal) stream is dominated by M inputs. A theory of attentional gating is proposed here where the M dominated dorsal stream gates the P inputs into the ventral stream. This framework is used to provide a neural explanation of the processes involved in reading and in learning to read. This scheme also explains how a magnocellular deficit could cause the common reading impairment, dyslexia.
authors.affiliation: Psychobiology Laboratory, Center for Visual Sciences, School of Psychology, Australian National University, Canberra, ACT 0200, Australia. sagar@anu.edu.au
authors.forename: T R
authors.initials: TR
authors.lastname: Vidyasagar
mesh_terms: D000818:Animals; D001288:Attention / Q000502:physiology*; D004410:Dyslexia / Q000503:physiopathology* / Q000523:psychology; D005246:Feedback; D006801:Humans; D008251:Macaca / Q000502:physiology*; D008568:Memory / Q000502:physiology; D008959:Models, Neurological; D010465:Perception / Q000502:physiology; D014793:Visual Cortex / Q000502:physiology*