NMDA neurotransmission as a critical mediator of borderline personality disorder.
Studies of the neurobehavioural components of borderline personality disorder (BPD) have shown that symptoms and behaviours of BPD are partly associated with disruptions in basic neurocognitive processes, in particular, in the executive neurocognition and memory systems. A growing body of data indicates that the glutamatergic system, in particular, the N-methyl-D-aspartate (NMDA) subtype receptor, plays a major role in neuronal plasticity, cognition and memory and may underlie the pathophysiology of multiple psychiatric disorders. In this paper, we review the literature regarding BPD and its cognitive deficits and the current data on glutamatergic and NMDA neurotransmission. We propose that multiple cognitive dysfunctions and symptoms presented by BPD patients, like dissociation, psychosis and impaired nociception, may result from the dysregulation of the NMDA neurotransmission. This impairment may be the result of a combination of biological vulnerability and environmental influences mediated by the NMDA neurotransmission.
Grosjean
Bernadette
B
Department of Psychiatry, Harbor-UCLA Medical Center, Torrance, California 90509, USA. bernaharbor@yahoo.com
Tsai
Guochuan E
GE
D001883:Borderline Personality Disorder / Q000175:diagnosis / Q000503:physiopathology* / Q000523:psychology / Q000628:therapy; D001921:Brain / Q000503:physiopathology; D003072:Cognition Disorders / Q000503:physiopathology; D006801:Humans; D008016:Life Change Events; D008569:Memory Disorders / Q000503:physiopathology; D016202:N-Methylaspartate / Q000819:agonists / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D011613:Psychotherapy; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000502:physiology*; D012307:Risk Factors; D012931:Social Environment; D009435:Synaptic Transmission / Q000502:physiology*
D016194:Receptors, N-Methyl-D-Aspartate; D016202:N-Methylaspartate