The impact acceleration (I/A) model of traumatic brain injury (TBI) was developed to reliably induce diffuse traumatic axonal injury in rats in the absence of skull fractures and parenchymal focal lesions. This model replicates a pathophysiology that is commonly observed in humans with diffuse axonal injury (DAI) caused by acceleration-deceleration forces. Such injuries are typical consequences of motor vehicle accidents and falls, which do not necessarily require a direct impact to the closed skull. There are several desirable characteristics of the I/A model, including the extensive axonal injury produced in the absence of a focal contusion, the suitability for secondary insult modeling, and the adaptability for mild/moderate injury through alteration of height and/or weight. Furthermore, the trauma device is inexpensive and readily manufactured in any laboratory, and the induction of injury is rapid (~45 min per animal from weighing to post-injury recovery) allowing multiple animal experiments per day. In this chapter, we describe in detail the methodology and materials required to produce the rat model of I/A in the laboratory. We also review current adaptations to the model to alter injury severity, discuss frequent complications and technical issues encountered using this model, and provide recommendations to ensure technically sound injury induction.
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http://dx.doi.org/10.1007/978-1-4939-3816-2_15 | DOI Listing |
ACS Nano
January 2025
Department of Biochemistry and Molecular Biology, School of Life Sciences, Central South University, Changsha 410078, Hunan, China.
Spinal cord injury (SCI) remains a formidable challenge in biomedical research, as the silencing of intrinsic regenerative signals in most spinal neurons results in an inability to reestablish neural circuits. In this study, we found that neurons with low axonal regeneration after SCI showed decreased extracellular signal-regulated kinase (ERK) phosphorylation levels. However, the expression of dual specificity phosphatase 26 (DUSP26)─which negatively regulates ERK phosphorylation─was reduced considerably in neurons undergoing spontaneous axonal regeneration.
View Article and Find Full Text PDFAdv Healthc Mater
January 2025
Department of Intelligent Precision Healthcare Convergence, Sungkyunkwan University (SKKU), Suwon, 16419, Republic of Korea.
Peripheral nerve injury is a common disease resulting in reversible and irreversible impairments of motor and sensory functions. In addition to conventional surgical interventions such as nerve grafting and neurorrhaphy, nerve guidance conduits are used to effectively support axonal growth without unexpected neuroma formation. However, there are still challenges to secure tissue-mimetic mechanical and electrophysiological properties of the conduit materials.
View Article and Find Full Text PDFTher Adv Neurol Disord
January 2025
Institute for Infectious Diseases, University of Bern, Bern, Switzerland.
Background: Serum neurofilament light chain (sNfL) is a biomarker for neuro-axonal injury.
Objectives: To assess sNfL's utility as a diagnostic marker for Lyme neuroborreliosis (LNB).
Methods: We compared serum and CSF NfL levels in LNB patients and age-matched controls.
Burns Trauma
January 2025
The Orthopaedic Center, The Affiliated Wenling Hospital of Wenzhou Medical University (The First People's Hospital of Wenling), 333 Chuanan Road, Chengxi Street, Wenling City, Zhejiang Province 317500, China.
Background: Neuronal structure is disrupted after spinal cord injury (SCI), causing functional impairment. The effectiveness of exercise therapy (ET) in clinical settings for nerve remodeling post-SCI and its underlying mechanisms remain unclear. This study aims to explore the effects and related mechanisms of ET on nerve remodeling in SCI rats.
View Article and Find Full Text PDFAnimal Model Exp Med
January 2025
School of Rehabilitation, Capital Medical University, Beijing, China.
Background: The inability of damaged neurons to regenerate and of axons to establish new functional connections leads to permanent functional deficits after spinal cord injury (SCI). Although astrocyte reprogramming holds promise for neurorepair in various disease models, it is not sufficient on its own to achieve significant functional recovery.
Methods: A rat SCI model was established using a spinal cord impactor.
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