Neuroplasticity in Post-Traumatic Stress Disorder

Abstract

Introduction: Post-traumatic stress disorder (PTSD) develops in response to a traumatic experience, whether real or threatening, which produces emotions of intense fear and memory problems, significantly damaging the quality of life of those who manifest it. In recent years, anatomical-functional changes in the amygdala-hippocampus-prefrontal cortex circuit have begun to be studied as a key factor in the prevention, vulnerability, and treatment of PTSD, with neuroplasticity being one of the factors of greatest interest. Therefore, this review will address the latest published data regarding PTSD and neuroplasticity.

Development: Data from preclinical and clinical models support that a traumatic experience modifies both synaptic plasticity through electrophysiological and chemical variables, as well as myelin plasticity which enables short and long-distance connections. This remodelling of circuitry is crucial for the development of PTSD. However, it is also closely associated with prevention and positive treatment outcomes. Variables such as social support or the use of psychotherapy following a traumatic experience are linked to a good prognosis.

Conclusions: Therefore, there is an interesting connection between neuroplasticity and PTSD, although many questions remain open today, along with promising lines of prevention and intervention, including psychedelic substances.

Keywords: PTSD; myelin; neuroplasticity; psychedelics; psychological trauma; synapses.

Fig. 1.

Representación esquemática de los factores que modulan la neuroplasticidad en personas con TEPT. Conjunto de factores y biomarcadores que interfieren en la neuroplasticidad y son claves en el desarrollo de TEPT. (A) Detalle de la plasticidad sináptica (verde BDNF, rojo oscuro receptor de BDNF TrkB, morado oscuro receptor AMPA y azul claro matriz extracelular). (B) Detalle de la plasticidad mielínica (morado claro oligodendrocito mielinizante). BDNF, factor neurotrófico derivado del cerebro; TrkB, receptor quinasa B de tropomiosina; AMPA, ácido $\alpha$-amino-3-hidroxi-5-metil-4-isoxa- zolpropiónico.