Reply to Stuart and Lovegrove's question, "visual processing deficits in dyslexia: receptors or neural mechanisms?"

Recently Stuart and Lovegrove questioned the receptor hypothesis of Grosser and Spafford which these authors used to account for the findings that dyslexic individuals have superior peripheral color discrimination to normal readers but also have poorer peripheral brightness discrimination than normal readers. Stuart and Lovegrove hypothesized that dyslexics instead have an impaired transient visual system. The receptor hypothesis is an attempt by Grosser and Spafford to link the functioning of the rods and cones to transient and sustained visual system functioning in a more specific manner than has been tried heretofore by suggesting that, while the parvocellular system is almost entirely fed by cones, both kinds of receptors drive magnocellular cells (but with the rapid onset of early transient system responding being due to the highly light sensitive rods). The rods are proposed to be the receptors initiating the rapid onset of responding in the magnocellular, transient pathway. In dyslexic individuals, they maintain, there are relatively fewer rods to provide for the rapid onset of transient system responses, resulting in a diminished capacity of the transient system to inhibit sustained system activity (as occurs with normal readers). Their receptor hypothesis supplements the concept of transient-vs-sustained system differences.