Isabella Harmath De Lemos
Research Mentor: Jonny Lifshitz
Mentor Department: Physical Medicine & Rehabilitation, Medicine
Author(s): Ema Schneiderhan, Isabella Harmath de Lemos, Lujaine Sadoun, Corey Stewart, L. Matthew Law, Jonathan Lifshitz
Session: Session 2 (10:00 AM – 10:50 AM)
Presentation Type: Poster 67
Abstract
Traumatic brain injury (TBI), caused by a sudden impact to the head or neck, is a major cause of disability and death in the United States. While most therapeutic efforts target the acute post-injury window—when neuroplasticity is naturally heightened—many individuals continue to experience chronic cognitive and neurological impairments long after the acute period has passed. Effective rehabilitation in the chronic stage requires re-engaging the injured brain into a more plastic, receptive state. Psychoplastogens, such as psilocybin, are a family of drugs that have emerged as promising candidates for inducing neuroplasticity. Psilocybin induces plasticity, yet its optimal dosing parameters after chronic TBI have not been defined. To investigate dose-dependent effects of psilocybin on neuroplasticity after chronic diffuse brain injury, we administered psilocybin at varying doses to rats one month post-fluid-percussion TBI–a clinically relevant model that produces persistent cognitive deficits. We hypothesized an optimal dose of psilocybin exists for each sex that increases spine density and dendritic arborization without sustained neurological signs. We harvested cortical tissue from TBI and sham rats and stained it using the Golgi method, and carried out a comparative analysis on the cortical brain regions be. Using the FIJI “Dendritic Spine Counter†plugin, we quantified spine head width, neck length, and neck width, classified spine morphology, and inferred maturity and synaptic connectivity. Data collection continues as spine analyses progress. This work will clarify whether psilocybin reactivates neuroplasticity in the chronically injured brain and may inform the development of novel interventions for persistent cognitive deficits following TBI.
