ts of dopamine agonists and anticholinergics can be similarly understood as affecting the relative precision of prior beliefs, as can the psychotomimetic effects of various drugs of abuse. 36 Psychedelic drugs like lysergic acid diethylamide (LSD), which act via serotonergic 5HT2A receptors, are potent inducers of visual hallucinations. 37 Blind subjects given LSD all experienced hallucinations in multiple modalities, although congenitally blind subjects did not report visual hallucinations. Of 13 late-blind subjects who experienced visual hallucinations, only two experienced complex hallucinations. 38 An in-depth account of LSD reported by a congenitally blind musician similarly reveals an absence of visual hallucinations but an abundance of experiences involving other senses. 39 Visual loss in later life is not protective against the development of schizophreniform psychosis. Indeed, in Usher syndrome, visual degeneration occurs after adolescence (although sometimes as early as in the first decade) and is associated with schizophrenia-like symptoms. 40–42 The Challenge Faced by the Developmentally Visually Deprived Brain For a congenitally blind person, there is no rich visual signal with which to shape one’s priors about the world. Each of the other sensory modalities samples a much smaller part of the sensorium, in a noisier fashion, and priors must be built up, piecemeal, from the information contained therein. It is essential then that these hard-won priors (both supramodal and within individual modalities 43 ) remain stable, so as to enable effective interaction within the world. That is, the organism should exhibit a relatively greater top-down influence of priors because the bottom-up, sensory information samples much less of it. As a congenitally blind individual walks down that same shopping street described above, his situation must be very different from a sighted individual with his eyes closed. The same auditory and tactile information that a blindfol