Serotonin axons in the neocortex of the adult female mouse regrow after traumatic brain injury
| Autor: | David J. Linden, Tymoteusz J. Kajstura, Sarah E. Dougherty |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Traumatic brain injury Central nervous system Neocortex Nerve Tissue Proteins Serotonergic Article Mice 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Brain Injuries Traumatic Glial Fibrillary Acidic Protein medicine Animals Axon Serotonin transporter biology business.industry Calcium-Binding Proteins Microfilament Proteins Nuclear Proteins medicine.disease Axons Nerve Regeneration Astrogliosis DNA-Binding Proteins Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure nervous system biology.protein Female Microglia Serotonin business Neuroscience 030217 neurology & neurosurgery Serotonergic Neurons |
| Zdroj: | Journal of Neuroscience Research. 96:512-526 |
| ISSN: | 0360-4012 |
| Popis: | It is widely held that injured neurons in the central nervous system do not undergo axonal regrowth. However, there is mounting evidence that serotonin axons are a notable exception. Serotonin axons undergo long-distance regrowth in the neocortex after amphetamine lesion and, following a penetrating stab injury, they can regrow from cut ends to traverse the stab rift. Traumatic brain injury (TBI) is clinically prevalent and can lead to pathologies such as depression that are related to serotonergic dysfunction. Thus, whether serotonin axons can regrow after TBI is an important question. We used two models for TBI, a persistent open skull condition and controlled cortical impact, to evoke injury in adult female mouse neocortex and assessed serotonin axon density one week, one month, and three months after injury by serotonin transporter immunohistochemistry. We found that following both forms of TBI, serotonin axon density is decreased posterior but not anterior to the injury site when measured in layer 1 at one week post-surgery, and that serotonin axons are capable of regrowing into the distal zone to increase density by one month post-surgery. This pattern is consistent with the anterior-to-posterior course of serotonin axons in the neocortex. TBI in these models is associated with significant reactive astrogliosis both anterior and posterior to the impact, but the degree of reactive astrogliosis is not correlated with serotonin axon density when measured one week after TBI. Microglial density remains constant following both types of injuries, but microglial condensation was detected one week after controlled cortical impact. |
| Databáze: | OpenAIRE |
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