title: A rapid lateral fluid percussion injury rodent model of traumatic brain injury and post-traumatic epilepsy.
abstract: Traumatic brain injury is a leading cause of acquired epilepsy. Initially described in 1989, lateral fluid percussion injury (LFPI) has since become the most extensively used and well-characterized rodent traumatic brain injury and post-traumatic epilepsy model. Universal findings, particularly seizures that reliably develop after an initial latent period, are evident across studies from multiple laboratories. However, the LFPI procedure is a two-stage process, requiring initial surgical attachment of a skull fluid cannula and then reanesthesia for delivery of the epidural fluid pressure wave. We now describe a modification of the original technique, termed 'rapid lateral fluid percussion injury' (rLFPI), which allows for a one-stage procedure and thus shorter operating time and reduced anesthesia exposure. Anesthetized male Long-Evans rats were subjected to rLFPI through a length of plastic tubing fitted with a pipette tip cannula with a 4-mm aperture. The cannula opening was positioned over a craniectomy of slightly smaller diameter and exposed dura such that the edges of the cannula fit tightly when pressed to the skull with a micromanipulator. Fluid percussion was then delivered immediately thereafter, in the same surgery session. rLFPI resulted in nonlethal focal cortical injury in all animals. We previously demonstrated that the rLFPI procedure resulted in post-traumatic seizures and regional gliosis, but had not examined other histopathologic elements. Now, we show apoptotic cell death confined to the perilesional cortex and chronic pathologic changes such as ipsilesional ventriculomegaly that are seen in the classic model. We conclude that the rLFPI method is a viable alternative to classic LFPI, and--being a one-stage procedure--has the advantage of shorter experiment turnaround and reduced exposure to anesthetics.
authors.affiliation: Departments of aNeurology bNeurosurgery, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA cDepartment of Neuroscience, Division of Clinical Neurophysiology, Uppsala University, Uppsala, Sweden dGraduate Institute of Neural Regenerative Medicine, Taipei Medical University, Taipei, Taiwan eDepartment of Infectious Diseases, Youan Hospital, Capital Medical University fDepartment of Neurology, Beijing Aerospace General Hospital, Beijing, China.
authors.forename: Mustafa Q
authors.initials: MQ
authors.lastname: Hameed
authors.forename: Grant S
authors.initials: GS
authors.lastname: Goodrich
authors.forename: Sameer C
authors.initials: SC
authors.lastname: Dhamne
authors.forename: Asa
authors.initials: A
authors.lastname: Amandusson
authors.forename: Tsung-Hsun
authors.initials: TH
authors.lastname: Hsieh
authors.forename: Danlei
authors.initials: D
authors.lastname: Mou
authors.forename: Yingpeng
authors.initials: Y
authors.lastname: Wang
authors.forename: Alexander
authors.initials: A
authors.lastname: Rotenberg
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000150:complications* / Q000209:etiology*; D002552:Cerebral Ventricles / Q000473:pathology; D004195:Disease Models, Animal; D004834:Epilepsy, Post-Traumatic / Q000209:etiology*; D005452:Fluoresceins; D020287:In Situ Nick-End Labeling; D008297:Male; D010474:Percussion / Q000295:instrumentation / Q000379:methods*; D051381:Rats; D020318:Rats, Long-Evans
chemical_list: D005452:Fluoresceins; C435731:fluoro jade