“…Although there is some evidence of an association between altered dopaminergic neurotransmission and psychometrically identified schizotypy (Woodward et al, 2011), findings are less consistent than in frank psychosis, possibly due to high heterogeneity in the experimental designs and methods used (Mohr & Ettinger, 2014). Moreover, elevated stress‐induced dopamine release as measured with [ 11 C]raclopride PET (Soliman et al, 2008) and increased functional activation as measured with functional MRI (Soliman et al, 2011) in striatal regions in schizotypy has only been observed in relation to negative schizotypal features (reflecting the interpersonal dimension of schizotypy, thought to mirror negative symptoms in schizophrenia), but not in relation to positive schizotypy (reflecting the cognitive‐perception dimension of schizotypy, thought to mirror positive symptoms in schizophrenia). Further research examining the relative contributions of hyperperfusion at different nodes of a hippocampal–striatal–midbrain circuit along a psychosis continuum (psychosis, CHR, and HS), combined with measurements of the different neurotransmitter systems involved (i.e., GABA, glutamate, and dopamine), may provide substantial insights into the neurobiology of risk and resilience for psychiatric disorders (Pantelis & Bartholomeusz, 2014).…”