Aim: The two main forms of traumatic spinal cord injury exist. The first type of injury occurs when mechanical forces compress blood vessels and damage both axons and neural membranes. The second type of injury occurs through pathophysiological and metabolic processes which start after the initial damage. Glutamate over-expression is an important secondary injury mechanism. We examined pregabalin's neuroprotective effect on ADNP (Activity Dependent Neuroprotective Factor) levels in a rat spinal cord injury model.Methods: The fourth Wistar male rats received random assignments to five distinct groups: the 1. grup (no any surgical approach), 2. group (laminectomy only), 3. group (spinal cord injury without medication), 4. group (spinal cord injury and the methylprednisolone treated), 5. group (spinal cord injury and the pregabaline treated group). Spinal cord injury was produced by climp compression. Functional evaluations were done using the inclined plane test and criteria of Drummond and Moore, evaluation of blood levels and tissue levels of ADNP were done by ELISA, and Immunohistochemistry. The glial cells and neural cells evaluated by Hematoxylin and eosin staining of tissue.Results: The results showed no important variations in motor function between different spinal cord injury groups (p=0.053). The pregabalin group had significantly higher neural cell counts (9.68 ± 3.58) than both group 3 (5.06 ± 2.55) and group 4 (6.80 ± 2.59) (p
Hasan İdiz (Sat,) studied this question.
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