After intense or prolonged use, drugs of abuse such as opiates, psychostimulants, and alcohol induce a neuroinflammatory response, which potentiates their reinforcing effects, contributing to the transition from controlled consumption to a compulsive pattern. Exposure to stress, particularly social stress, acts as a critical variable in the initiation, maintenance, or relapse of drug use. There is currently abundant scientific evidence of the close relationship between stress, drug use, and the development of neuroinflammation. Studies with animal models have shown that social stress acts as a potent modulator of the immune system, promoting the activation of microglia and the release of proinflammatory cytokines such as IL-1β, IL-6, and TNF-α. This inflammatory response alters neuronal homeostasis, affecting key regions involved in the brain’s reward system and executive control, such as the nucleus accumbens, the amygdala, and the prefrontal cortex. Social stress is a critical variable in the development of SUD. It can activate the immune system, causing neuroinflammation and establishing a pathological circuit between the reward system and the prefrontal cortex. Pharmacological interventions that modulate the brain’s immune response offer new strategies to prevent or treat addiction, especially in individuals with high vulnerability to stress. Natural or synthetic substances with antioxidant and anti-inflammatory properties offer promising results. These preclinical findings highlight the importance of neuroinflammation and stress in understanding addictive behavior.
Keywords:
Neuroinflammation, drugs, stress.
Authors
Financing
PID-2020-112672RB-100/AEI, Ministerio de Universidades e Investigación RIAPAD, RD21/0009/0005/, RD24/0003/0004 Instituto de Salud Carlos III. CIPROM/ 2021/080/ Conselleria de Educación, Cultura, Universidades y Empleo.
