European Behavioural Pharmacology Society

@eurbehavpharm.bsky.social

The European Behavioural Pharmacology Society- an international society at the crossroads of pharmacology, experimental psychology, psychiatry & neuroscience.

Thank you to our speakers and everyone who joined this morning's EBBS/EBPS joint event. We look forward to seeing you around at the FENS Forum over the coming days!

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🚨 A reminder, The deadline for our travel awards is fast approaching. Submit your application by May 5th to be considered. Travel awards will be up to €750 to support workshop attendance. #EBPS2026

European Behavioural Pharmacology Society@eurbehavpharm.bsky.social · 5mo ago

We are accepting Travel Award applications for #EBPS2026. We are especially interested in applications from trainees from underrepresented backgrounds. All details can be found on the event website ebps2026.azuleon.org/information#...

Great to see Felippe Espinelli Amorim’s (not yet on BlueSky) and @charlotte-rye.bsky.social’s meta-analysis on mitochondrial dysfunction in PTSD out in @psychopharmacology.bsky.social 👏🏻 link.springer.com/article/10.1...

Mitochondrial dysfunction in PTSD: A mechanism to understand trauma susceptibility? - Psychopharmacology

Rationale and Objectives Post-Traumatic Stress Disorder (PTSD) is a complex mental health condition that arises following exposure to traumatic events. Converging evidence suggests mitochondrial dysfunction and brain energy metabolism impairment in its pathophysiology. Thus, examining mitochondrial data from both preclinical and experimental medicine studies may help us to have a deeper understanding of the pathophysiological mechanisms underlying PTSD. Methods Using PubMed, Scopus and Web of Science online databases, we conducted a search for peer-reviewed manuscripts targeting both mitochondrial-related activity and PTSD. Our search yielded 43 studies in total, including 29 in rodent models and 15 clinical studies. Results Preclinical studies reported a decrease in energy metabolism with a reduction in adenosine triphosphate (ATP) level, upregulation of genes associated with ATP synthesis, impairment of the glycolytic pathway, citric acid cycle and oxidative phosphorylation pathways and increased oxidative stress and neuronal apoptosis in the brain, or systemically. In the clinical setting, studies identified 1108 participants with PTSD and 312 with partial PTSD, with these individuals showing alterations in energy production, mitochondrial DNA copy number (mtDNAcn) and elevated oxidative stress. Risperidone and AC-5216—a selective ligand for TSPO—emerged as potential treatments. Conclusion Our synthesis of the published findings indicates a notable overlap between results from both animal models and humans which could show a potential usage of mitochondrial-related targets as biomarkers or for drug discovery. Additionally, these results highlight the need for future research in describing whether mitochondrial dysfunction is a cause or a symptom of PTSD.

link.springer.com

Dear EBPS community, we have published our latest newsletter with up to date goings on, and future events. We have included new content, including a "Perspectives" and "Industry Updates" piece for your interest. You can download the newsletter here drive.google.com/file/d/1f8t_...

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