The interpersonal dimension of borderline personality disorder: toward a neuropeptide model

Abstract

Borderline personality disorder is characterized by affective instability, impulsivity, identity diffusion, and interpersonal dysfunction. Perceived rejection and loss often serve as triggers to impulsive, suicidal, and self-injurious behavior, affective reactivity, and angry outbursts, suggesting that the attachment and affiliative system may be implicated in the disorder. Neuropeptides, including the opioids, oxytocin, and vasopressin, serve a crucial role in the regulation of affiliative behaviors and thus may be altered in borderline personality disorder. While clinical data are limited, the authors propose alternative neuropeptide models of borderline personality disorder and review relevant preclinical research supporting the role of altered neuropeptide function in this disorder in the hope of stimulating more basic research and the development of new treatment approaches.

Figure 1. Neuropeptide Modulation of Cortical and Limbic Function

Figure 2. Model of Opioid Dysfunction and Buprenorphine Treatment in Borderline Personality Disorder^a

^aBasal opioid levels in borderline personality disorder are hypothesized to be reduced in output, while receptors are increased in number, so that during unstimulated conditions, borderline patients experience dysphoria associated with reduced tonic opioid activity. When stress or pain causes an increase in release of opioids, there is an increased opioid signal and relief from dysphoria. Treatment with buprenorphine, a partial agonist, would increase basal opioid signal under baseline conditions of low tonic activity and antagonize opioid receptors under conditions of increased output (e.g., self-injurious behavior).