In April 2025, Acharya et al. published a pivotal study for therapeutic intervention in traumatized subjects. The research team demonstrated that administering Osanetant—a neurokinin-3 receptor (Nk3R) antagonist—significantly reduced freezing behavior in female mice during fear expression, suggesting a diminished consolidation of traumatic memory. This finding opens the possibility of using Osanetant as an immediate pharmacological intervention in emergency settings to prevent the development of Post-Traumatic Stress Disorder (PTSD).
This presentation aims to critically examine the epistemological assumptions underlying such neuroscientific developments. Framed within the dominant etiological model of cerebrality (Malabou, 2019), these advances imply a specific causal and semantic stance toward the psychological, where cerebral representation is privileged as the primary therapeutic target. This somatogenic perspective reveals a position in what Malabou has called a "fratricidal war for etiological dominance."
Drawing on the problematic relationship between psyche and event, and revisiting historical debates on psychological trauma from the 19th and 20th centuries, we argue that these disputes remain relevant for assessing emerging treatments. The notion of psychogenicity, often sidelined in favor of neurobiological explanations, will be reexamined in light of contemporary pharmacological strategies.
Finally, we explore a hypothetical scenario in which Osanetant-based intervention becomes viable in clinical practice. This raises ethical dilemmas concerning memory modulation, personal identity, and informed consent. If memory can be pharmacologically altered shortly after a traumatic event, what implications does this have for the subject's narrative continuity and autonomy?
By situating this scientific development within broader philosophical and psychological debates, the presentation seeks to contribute to a more nuanced understanding of trauma treatment and its epistemological and ethical foundations.
