Schizophrenia seen as a deficit in the modulation of cortical minicolumns by monoaminergic systems

Abstract

The highly evolved architecture of the cerebral cortex is organized across hierarchical levels that maximize functional repertoires (emergent properties) and expedite information processing. Minicolumns are nested within this multiscale architecture as the smallest module capable of processing information. Signals are transmitted within minicolumns through massive ion-gated connections and modulated through slower onset second messenger systems. The terminal zones of the modulatory second messenger systems comprise the laminae of the cortex. A comprehensive review of the literature suggests that schizophrenia results from widely distributed changes at the level of the cerebral cortex and little, if any, neuronal somatic changes: (Esiri & Crow, ). Concordant with this observation recent studies indicate that schizophrenic patients have an alteration of neuronal connectivity according to both lamina and brain region examined. One possible explanation for this deficit is an alteration in the modulatory system of cortical minicolumns. This ontogenetic deficit propitiates a cascade of neurochemical changes resulting in varying abnormalities relating information processing to behavioural states.