Journal of psychiatric research · 2026
Glutamatergic neurotransmission in violence and psychosis: an LTP-like cortical plasticity study.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Bang Nina, Berg Nesset Merete, Rasmussen Kirsten, Dahl Hilde, Bell Christina, Fischer-Vieler Thomas, Friestad Christine, Andreassen Ole A, Moberget Torgeir, Jönsson Erik G, Haukvik Unn K, Elvsåshagen Torbjørn
Аннотация
BACKGROUND: Among the various mechanisms implicated in abnormal aggression and violent behavior, impaired glutamatergic neurotransmission may represent one contributing factor. However, this hypothesis has been insufficiently explored in human studies.
METHODS: The purpose of the present study was to investigate associations between violent behavior in individuals with and without psychosis and electroencephalography (EEG)-based measures of long-term potentiation (LTP)-like plasticity of the visually evoked potential (VEP), which was previously linked to glutamatergic neurotransmission. Here, healthy controls (HC, n = 180), individuals with psychosis and history of aggression and violent behavior (violent-PSY, n = 16), individuals with psychosis without a history of violence (nonviolent-PSY, n = 25), and individuals with a history of violence without psychosis (violent non-PSY, n = 23) underwent EEG and clinical assessments.
RESULTS: Plasticity of VEP component P2 was significantly reduced in violent-PSY compared to nonviolent-PSY (P = .004). Plasticity of P1 component was reduced in violent non-PSY compared to HCs (P = .031). There was no significant association between VEP plasticity and clinical measures of psychotic symptoms, global functioning, and psychopathic traits.
CONCLUSIONS: Our findings suggest that synaptic plasticity-the adaptive strengthening or weakening of synaptic connections-may be reduced in patients with psychosis and in individuals with a history of violence. Further research is needed to clarify whether plasticity of the P2 component may serve as a marker of violent behavior in psychosis.
METHODS: The purpose of the present study was to investigate associations between violent behavior in individuals with and without psychosis and electroencephalography (EEG)-based measures of long-term potentiation (LTP)-like plasticity of the visually evoked potential (VEP), which was previously linked to glutamatergic neurotransmission. Here, healthy controls (HC, n = 180), individuals with psychosis and history of aggression and violent behavior (violent-PSY, n = 16), individuals with psychosis without a history of violence (nonviolent-PSY, n = 25), and individuals with a history of violence without psychosis (violent non-PSY, n = 23) underwent EEG and clinical assessments.
RESULTS: Plasticity of VEP component P2 was significantly reduced in violent-PSY compared to nonviolent-PSY (P = .004). Plasticity of P1 component was reduced in violent non-PSY compared to HCs (P = .031). There was no significant association between VEP plasticity and clinical measures of psychotic symptoms, global functioning, and psychopathic traits.
CONCLUSIONS: Our findings suggest that synaptic plasticity-the adaptive strengthening or weakening of synaptic connections-may be reduced in patients with psychosis and in individuals with a history of violence. Further research is needed to clarify whether plasticity of the P2 component may serve as a marker of violent behavior in psychosis.