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Tacrolimus (fk-506) Improves Sensory Nerve Regeneration
PN Afrooz, KM Washington, EE Kwegyir-Afful, DJ Simons, WP Andrew Lee
University of Pittsburgh Medical Center
2012-02-15
Presenter: Rami Zanoun
Affidavit:
This project is the sole product of Rami Zanoun, a medical student at the University of Pittsburgh School of Medicine. He completed this study in colaboration with his co-authors.
Director Name: Joseph Losee
Author Category: Student
Presentation Category: Basic Science Research
Abstract Category: Hand
How does this presentation meet the established conference educational objectives?
This is a novel study assessing the OBJECTIVE effect of tacrolimus on sensory regeneration in a rodent model. Most studies in the literature have subjective ways of measuring sensory regeneration. For this reason, when functional recovery is described in the literature, motor function is highlighed and return of sensation is often not characterized.
How will your presentation be used by practicing physicians in the audience?
As this is a basic science project, it will hopefully provide a basis for future research in sensory recovery after injury.
Background: Peripheral nerve injuries remain a challenging surgical problem. The immunosuppressive agent Tacrolimus (FK506) has been shown to increase the rate of axonal regeneration in motor nerves. In this study neuronal response properties were utilized to objectively evaluate effects of FK506 on sensory regeneration after nerve transaction and repair. Methods: Ten Lewis rats (250-300 grams) underwent transection and repair of the left infraorbital nerve. The first five received daily IP injections of FK506 at a dose of 2mg/kg. The second five received no treatment and served as a negative control. A third group of five additional rats served as naive controls. Extracellular Trigeminal Ganglion (TG) recordings were obtained during controlled whisker stimulation at 4 weeks thereafter. TG neuronal response properties were quantified using specialized software. Histomorphometric analysis was performed for all groups. Results: Maximal response magnitude, which measures axonal integrity, returned to control levels. The percentage of slowly adapting cells, measuring fine touch discrimination, in animals treated with FK506 returned to control levels (50%) compared to no-treatment group (30%). Neuronal latency, which is inversely related to axonal myelination, diminished with FK506 treatment and was significantly different than no- treatment group -- but didn't attain control levels. Maximal response magnitude and neuronal latency in the treated group were equivalent to animals after 8 weeks of recovery without any treatment. Conclusion: Systemic FK506 at a dose of 2mg/kg after transection and repair of a sensory nerve in Lewis rats reduces recovery time by nearly half as measured by certain aspects of electrophysiology.
