Abstract
Schizophrenia is a chronic disorder characterized by specific positive and negative primary symptoms, social behavior disturbances and cognitive deficits (e.g., impairment in working memory and cognitive flexibility). Mounting evidence suggests that altered excitability and inhibition at the molecular, cellular, circuit and network level might be the basis for the pathophysiology of neurodevelopmental and neuropsychiatric disorders such as schizophrenia. In the past decades, human and animal studies have identified that glutamate and gamma-aminobutyric acid (GABA) neurotransmissions are critically involved in several cognitive progresses, including learning and memory. The purpose of this review is, by analyzing emerging findings relating to the balance of excitatory and inhibitory, ranging from animal models of schizophrenia to clinical studies in patients with early onset, first-episode or chronic schizophrenia, to discuss how the excitatory-inhibitory imbalance may relate to the pathophysiology of disease phenotypes such as cognitive deficits and negative symptoms, and highlight directions for appropriate therapeutic strategies.
Highlights
Schizophrenia is a chronic, debilitating disorder characterized by primary symptoms, social and behavioral disturbances, and cognitive deficits
The gamma-aminobutyric acid (GABA) levels increased with age, duration of illness, and with therapy of long-term neuroleptic
Several factors are highly likely to contribute to E-I imbalance, including developmental alterations, as well as alterations at the cell, circuit, network and receptor levels; the variety of factors might be the reason for the heterogeneity in clinical, cognitive, social, and behavioral phenotypes of schizophrenia patients
Summary
Schizophrenia is a chronic, debilitating disorder characterized by primary symptoms (positive and negative), social and behavioral disturbances, and cognitive deficits. Neural information consists of both excitatory signals from glutamatergic pyramidal neurons and inhibitory signals originate from GABAergic interneurons. Maintenance of the balance of excitatory and inhibitory signals is critical for the development and function of cortical microcircuits and neural networks. Disruption of this finely tuned excitatory-inhibitory (E-I) balance has been proposed as a hypothesis providing insights into the pathomechanisms underlying neurodevelopmental and neuropsychiatric disorders (Rubenstein and Merzenich, 2003; Yizhar et al, 2011; Lisman, 2012)
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