The schizotypy construct focuses attention on the liability to develop schizophrenia-spectrum disorders, yet traditionally, the schizotypy models have put more emphasis on stress-vulnerability interactions rather than developmental dynamics of emerging risk for psychopathology. Indeed, developmental accounts of this emerging personality trait have rarely been explicitly formulated. In this position article, we wish to convey some of the basic developmental tenets of schizotypy, and how they can inform high-risk research. Firstly, we tackle the state vs trait issue to outline the possible relationship between high-risk states and trait schizotypy. Second, we review the evidence suggesting that the consolidation of schizotypy, encompassing its 3 main dimensions, could be considered as a developmental mediator between very early risk factors and transition into high-risk states. Importantly, developmental dynamics between endophenotypes, as well as transactional and epigenetics mechanisms should enter modern conceptualizations of schizotypy. Finally, we present a developmental psychopathology perspective of schizotypy sensitive to both the multifinality and equifinality of schizophrenia-spectrum disorders. We conclude that schizotypy represents a crucial construct in a fully-developmental study of schizophrenia-spectrum disorders.

This review from the International Consortium on Hallucinations Research intends to question the pertinence of the excitatory-to-inhibitory (E/I) imbalance hypothesis as a model for hallucinations. A large number of studies suggest that subtle impairments of the E/I balance are involved in neurological and psychiatric conditions, such as schizophrenia. Emerging evidence also points to a role of the E/I balance in maintaining stable perceptual representations, suggesting it may be a plausible model for hallucinations. In support, hallucinations have been linked to inhibitory deficits as shown with impairment of gamma-aminobutyric acid transmission, N -methyl- d -aspartate receptor plasticity, reductions in gamma-frequency oscillations, hyperactivity in sensory cortices, and cognitive inhibition deficits. However, the mechanisms by which E/I dysfunctions at the cellular level might relate to clinical symptoms and cognitive deficits remain unclear. Given recent data advances in the field of clinical neuroscience, it is now possible to conduct a synthesis of available data specifically related to hallucinations. These findings are integrated with the latest computational frameworks of hallucinations, and recommendations for future research are provided.