Changes in microglial cell numbers in the spinal cord dorsal horn following brachial plexus transection in the adult rat

Cova, John L.; Aldskogius, Håkan; Arvidsson, Jan; Molander, Carl

doi:10.1007/bf00279661

Cited by 27 publications

(14 citation statements)

References 30 publications

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“…There was no significant difference in microglial cell number between unaffected side (i.e., ipsilateral to the lesion) in the PTX group compared with uninjured sham (p = 0.39 to 0.84). Together, these findings suggest that, like other selective nerve injury models (Blackbeard et al, 2007; Block et al, 2005; Cova et al, 1988), microgliosis is topographically related to the loss of CST axon terminations and not a generalized inflammatory response.…”

Section: Resultsmentioning

confidence: 60%

Selective Corticospinal Tract Injury in the Rat Induces Primary Afferent Fiber Sprouting in the Spinal Cord and Hyperreflexia

et al. 2012

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The corticospinal tract (CST) has dense contralateral and sparse ipsilateral spinal cord projections that converge with proprioceptive afferents on common spinal targets. Previous studies in adult rats indicate that the loss of dense contralateral spinal CST connections after unilateral pyramidal tract section (PTX), which models CST loss after stroke or spinal cord injury, leads to outgrowth from the spared side into the affected, ipsilateral, spinal cord. The reaction of proprioceptive afferents after this CST injury, however, is not known. Knowledge of proprioceptive afferent responses after loss of the CST could inform mechanisms of maladaptive plasticity in spinal sensorimotor circuits after injury. Here we hypothesize that the loss of the contralateral CST results in a reactive increase in muscle afferents from the impaired limb and enhancement of their physiological actions within the cervical spinal cord. We found that ten days after PTX, proprioceptive afferents sprout into cervical gray matter regions denervated by the loss of CST terminations. Further, VGlut1 positive boutons, indicative of group 1A afferent terminals, increased on motoneurons. PTX also produced an increase in microglial density within the gray matter regions where CST terminations were lost. These anatomical changes were paralleled by reduction in frequency-dependent depression of the H-reflex, suggesting hyperreflexia. Our data demonstrate for the first time that selective CST injury induces maladaptive afferent fiber plasticity remote from the lesion. Our findings suggest a novel structural reaction of proprioceptive afferents to the loss of CST terminations and provide insight into mechanisms underlying spasticity.

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Section: Resultsmentioning

confidence: 60%

Selective Corticospinal Tract Injury in the Rat Induces Primary Afferent Fiber Sprouting in the Spinal Cord and Hyperreflexia

et al. 2012

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“…The presence of reactive astrocytes in the dorsal gray matter is strongly supportive of the idea that the glial reactions observed in this area within a few days followinginjury to branches ofspinal nerves (Cova et al, 1988;Gilmore, 1975;Gilmore and Skinner, 1979;Gilmore and Walls, 1981) are related to alterations induced in the central processes of dorsal root ganglion neurons. In the present study, the astrocytic response in the dorsal gray matter is clearly present and unequivocal by the second day following axotomy.…”

Section: Discussionmentioning

confidence: 69%

Astrocytic reactions in spinal gray matter following sciatic axotomy

Gilmore

Sims

Leiting

1990

Glia

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Astrocytic responses following unilateral sciatic nerve axotomy were examined in the spinal gray matter. Using an antiserum to glial fibrillary acidic protein (GFAP), immunoreactive astrocytes were studied in both dorsal and ventral gray matter at intervals from 2 days through 34 days post-axotomy. In all axotomized animals, increased numbers of strongly immunoreactive astrocytes were present in the gray matter ipsilateral to the surgery. Such astrocytes were absent from the contralateral intact side and from gray matter bilaterally in adjacent spinal segments not involved in formation of the sciatic nerve. These GFAP-positive astrocytes occurred not only in association with large motor neurons in the ventral gray matter but also in association with central processes of dorsal root ganglion neurons in the dorsal gray matter. The response was quite rapid, being discernible both dorsally and ventrally as early as the second post-operative day. This increased GFAP immunoreactivity persisted throughout the entire observation period, with the perikarya of large ventral motor neurons appearing to become surrounded or encapsulated by the immunoreactive processes. A further alteration noted at the longest post-operative intervals was the presence in the ventral gray matter of astrocytes appearing to be binucleate. The data obtained indicate that the astrocytic response is not related solely to reactions in motor neurons and, furthermore, the rapidity with which it develops in the dorsal gray matter suggests that its induction is not dependent upon transganglionic degeneration, which others have reported to occur weeks after peripheral nerve injury.

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“…Most data on the microglial response to axotomy have been derived from studies in cranial nerves (e.g., Sjös-trand, 1971;Torvik and Søreide, 1975;Aldskogius, 1982;Svensson and Aldskogius, 1993) or peripheral nerves (e.g., Kerns and Hinsman, 1973;Cova et al, 1988;Eriksson et al, 1993;Lu and Richardson, 1993). In particular, changes in microglial cells after transection of the facial nerve were investigated extensively by Kreutzberg and coworkers (Blinzinger and Kreutzberg, 1968;Streit and Kreutzberg, 1987;Graeber et al, 1988a,b;Streit and Graeber, 1993).…”

Section: Postlesional Microglial Activation Varies With the Lesion Pamentioning

confidence: 99%

Region-specific activation of microglial cells in the rat septal complex following fimbria-fornix transection

et al. 1998

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Studies of postlesional microglial activation may gain insight into microglia/neuronal interactions in processes of neurodegeneration. We compared the microglial response after axotomy of septohippocampal projection neurons with that seen after selective immunolesioning of cholinergic septohippocampal neurons with the immunotoxin 192 IgG-saporin. Using the microglial marker isolectin B4 from Griffonia simplicifolia (GSA I-B4), we found striking differences in the microglial response between these two lesion paradigms. Following axotomy of septohippocampal neurons by fimbria-fornix transection (ff-t), there was only a moderate and short-lasting microglial reaction in the medial septum (MS) in the early postlesion period. Prelabeling of septohippocampal neurons with Fluoro-Gold (FG) prior to axotomy revealed the survival of most neurons, and only very rarely were microglial cells observed that had phagocytosed FG-labeled debris. In the lateral septum (LS) containing the degenerating terminals of hippocamposeptal fibers transected by ff-t, a heavy reaction of lectin-labeled activated microglial cells associated with high phagocytotic activity was noticed. Unexpectedly, after a long survival time (6 months) following ff-t, we observed an increase in microglial GSA I-B4 labeling in the MS. In contrast, an inverse pattern of the microglial response, i.e., a strong initial reaction in the MS and very little microglial activation in the LS, was observed after immunolesioning. Our results indicate that the microglial reaction in the MS following ff-t differs substantially from that seen in other models of axotomy.

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Changes in microglial cell numbers in the spinal cord dorsal horn following brachial plexus transection in the adult rat

Cited by 27 publications

References 30 publications

Selective Corticospinal Tract Injury in the Rat Induces Primary Afferent Fiber Sprouting in the Spinal Cord and Hyperreflexia

Selective Corticospinal Tract Injury in the Rat Induces Primary Afferent Fiber Sprouting in the Spinal Cord and Hyperreflexia

Astrocytic reactions in spinal gray matter following sciatic axotomy

Region-specific activation of microglial cells in the rat septal complex following fimbria-fornix transection

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