Glutamatergic neurotransmission in violence and psychosis: an LTP-like cortical plasticity study

J Psychiatr Res. 2026 Apr 25;199:122-129. doi: 10.1016/j.jpsychires.2026.04.017. Online ahead of print.

ABSTRACT

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.

PMID:42056809 | DOI:10.1016/j.jpsychires.2026.04.017