![]() ![]() In parallel, the ability of psychostimulants, such as amphetamine, to induce schizophrenia-like psychotic symptoms was found to be tied to their stimulatory effects on dopaminergic systems in the brain 152. These effects were later tied to the blockade of D2-type dopamine receptors 151. The dopamine model is based on the fortuitous observation that the compound chlorpromazine had dramatic and unexpected effects on symptoms of schizophrenia 150. ![]() Currently, there are two major neurochemical models for this disorder: the dopaminergic and glutamatergic models. The aetiological mechanisms of schizophrenia remain unclear. Model psychoses and neurochemical conceptualizations of schizophrenia We also consider how auditory deficits might relate to existing neurochemical theories of schizophrenia 6, 7 ( BOX 1). Subsequently, we review the structural evidence for auditory cortical involvement in schizophrenia, especially from post-mortem investigations 5, and highlight both the convergences and divergences between the functional and structural findings. We then discuss the mechanisms by which auditory cortical dysfunction leads to the characteristic behavioural manifestations of schizophrenia, especially the impairments in social interaction and communication skills that are tied directly to poor psychosocial function in schizophrenia. Neurophysiological approaches, including event-related potential (ERP) and event-related spectral perturbation (ERSP) techniques, have proved particularly effective both for characterizing the clinical deficits in schizophrenia 2, 3 and for linking them to underlying pathogenic mechanisms 4, and we thus describe them in detail. In this Review, we first discuss the evidence for auditory sensory dysfunction in schizophrenia and its underlying mechanisms, particularly the contribution of NMDA receptor (NMDAR) dysfunction and related impairments in glutamatergic and GABAergic function. In addition, these deficits contribute substantially to symptoms and overall impairments in psychosocial function. A key goal of current schizophrenia research, therefore, has been to determine the neural mechanisms underlying these deficits to guide future interventional approaches.Īlthough neurocognitive studies of schizophrenia have traditionally focused on higher-order functions such as working memory and executive processing, basic sensory functions - including auditory-level function - are also impaired in this disorder and may be particularly amenable to translational, cross-species research. At present, there are no approved treatments that specifically target the neurocognitive impairments in schizophrenia. The onset of schizophrenia is typically in late adolescence or early adulthood in males (age 17–21 years) and somewhat later in females, and the disorder is associated with lifelong disability thereafter 1. ![]() In general, patients with this disorder show a deficit of 1–2 standard deviations in cognitive function, corresponding to a mean reduction in performance IQ to 70–85 (versus the normative value of 100) 2. Nevertheless, the impaired psychosocial outcome in schizophrenia is driven primarily by deficits in neurocognitive functions that are manifest across a wide range of cognitive domains. It is diagnosed primarily based on common clinical manifestations, such as agitation, paranoia, delusions and hallucinations (the ‘positive’ symptoms), and/or apathy, social withdrawal and anhedonia (the ‘negative’ symptoms). Schizophrenia is a severe psychiatric disorder that affects ~1% of the population worldwide 1. ![]()
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