This concept describes the balance between cortical excitation and inhibition that the review treats as a key intermediate mechanism in schizophrenia.
First-pass extracted concept
cortical excitation-inhibition balance
Candidate: concept label2 source documents6 linked claims
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Aliases
E/I balance, imbalanced excitatory and inhibitory output
Extracted Explainers
Evidence Snippets
Early stages of Huntington's disease (HD) before the onset of motor and cognitive symptoms are characterized by imbalanced excitatory and inhibitory output from the cortex to striatal and subcortical structures.
There have been considerable advances in our understanding of the normal neurodevelopmental refinement of synapses and cortical excitation-inhibition (E/I) balance.
Supporting Sources
Linked Claims
Early presymptomatic Huntington's disease is characterized by imbalanced excitatory and inhibitory cortical output to striatal and subcortical structures.
Quoted textsource-backed
Early stages of Huntington's disease (HD) before the onset of motor and cognitive symptoms are characterized by imbalanced excitatory and inhibitory output from the cortex to striatal and subcortical structures.
The presymptomatic window in Huntington's disease may allow microcircuit firing-rate adjustment to restore impaired excitation/inhibition balance and thereby prevent or slow disease progression.
Quoted textsource-backed
The window before the onset of symptoms presents an opportunity to adjust the firing rate within microcircuits with the goal of restoring the impaired E/I balance, thereby preventing or slowing down disease progression.
The integrated hypothesis proposes that frontal cortical excitation-inhibition imbalance can disinhibit excitatory projections regulating mesostriatal dopamine neurons, leading to dopamine dysregulation and psychotic symptoms.
The integrated hypothesis proposes that overpruning of synapses, including glutamatergic inputs onto frontal cortical interneurons, disrupts cortical excitation-inhibition balance and contributes to cognitive and negative symptoms.
The abstract states that schizophrenia is associated with variants linked to genes affecting GABA signaling, glutamatergic signaling, and neurodevelopmental processes.
The review argues that schizophrenia evidence can be integrated through a model linking neurodevelopmental synaptic refinement abnormalities, cortical excitation-inhibition imbalance, and dopaminergic dysfunction.