ArticleAutonomic neuroscience : basic & clinical2012
Transient changes in spinal cord glial cells following transection of preganglionic sympathetic axons.
Article in Autonomic neuroscience : basic & clinical, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Activated Microglia in the Rat Spinal Cord Following Peripheral Axon Injury Promote Glial and Neuronal Plasticity Which is Necessary for Long-Term Neuronal Survival.Cellular and molecular neurobiology · 2021Article
- Elimination of microglia in mouse spinal cord alters the retrograde CNS plasticity observed following peripheral axon injury.Brain research · 2019Article
- Retrograde influences of SCG axotomy on uninjured preganglionic neurons.Brain research · 2018Article
- Increased Cx32 expression in spinal cord TrkB oligodendrocytes following peripheral axon injury.Neuroscience letters · 2016Article
- Distribution and phenotype of TrkB oligodendrocyte lineage cells in the adult rat spinal cord.Brain research · 2014Article
- Transection of preganglionic axons leads to CNS neuronal plasticity followed by survival and target reinnervation.Autonomic neuroscience : basic & clinical · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Following peripheral nerve injury, retrograde signals originating from the injury site may activate intrinsic factors in the injured neurons, possibly leading to regenerative growth. Retrograde influences from peripheral injury sites may lead to the activation of glial cells in the vicinity of the centrally located cell bodies of the injured neurons. Few studies have examined changes in the spinal cord intermediolateral cell column (IML), which houses sympathetic preganglionic cell bodies, following injury to distal axons in the cervical sympathetic trunk (CST). The goal of the present study was to determine if transection of the CST results in plasticity in glial cells in the IML. At 1 day following injury, changes in the expression of microglial marker Iba1 were observed and the typical oligodendrocyte-neuronal relationship was altered. By 7 days, astrogliosis, microglial aggregation, and increased numbers of oligodendrocytes, as well as enhanced glial-glial and glial-neuronal relationships were present. The majority of cases were similar to controls at 3 weeks following injury and no changes were observed in any cases at 10 weeks following the injury. These results revealed changes in astrocytes, microglia, oligodendrocytes in the spinal cord following transection of preganglionic axons comprising the CST, indicating their ability to respond to distal axonal injury.
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