Magnocellular and parvocellular contributions to brain network dysfunction during learning and memory: Implications for schizophrenia.

Memory deficits are core features of schizophrenia, and a central aim in biological psychiatry is to identify the etiology of these deficits. Scrutiny is naturally focused on the dorsolateral prefrontal cortex and the hippocampal cortices, given these structures' roles in memory and learning. The fronto-hippocampal framework is valuable but restrictive. Network-based underpinnings of learning and memory are substantially diverse and include interactions between hetero-modal and early sensory networks. Thus, a loss of fidelity in sensory information may impact memorial and cognitive processing in higher-order brain sub-networks, becoming a sensory source for learning and memory deficits. In this overview, we suggest that impairments in magno- and parvo-cellular visual pathways result in degraded inputs to core learning and memory networks. The ascending cascade of aberrant neural events significantly contributes to learning and memory deficits in schizophrenia. We outline the network bases of these effects, and suggest that any network perspectives of dysfunction in schizophrenia must assess the impact of impaired perceptual contributions. Finally, we speculate on how this framework enriches the space of biomarkers and expands intervention strategies to ameliorate this prototypical disconnection syndrome.