Combined Genetic Attenuation of Myelin and Semaphorin-Mediated Growth Inhibition Is Insufficient to Promote Serotonergic Axon Regeneration

Lee, Jae K.; Chow, Renée; Xie, Fang; Chow, Sharon Y.; Tolentino, Kristine; Zheng, Binhai

doi:10.1523/jneurosci.2269-10.2010

Cited by 71 publications

(58 citation statements)

References 37 publications

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“…Rosa26-tdTomato reporter mice were kindly donated by Dr. Fan Wang, Duke University, Durham, NC (Lee et al, 2009). All mice had pure C57BL/6 genetic background.…”

Section: Methodsmentioning

confidence: 99%

“…To generate Col1␣1/NG2 mice for genetic lineage tracing studies, the three mouse lines were bred to each other to produce Col1␣1-GFP ϩ /NG2-CreER ϩ /Rosa26-tdTomato fl/ϩ offspring. Col1␣1/NG2 mice (6 -7 weeks old) received tamoxifen as previously described (Lee et al, 2009). One week after the last injection, mice were subjected to SCI.…”

Section: Methodsmentioning

confidence: 99%

“…before receiving mid-thoracic (T8) spinal cord injuries. Dorsal hemisections were performed as previ-ously described (Lee et al, 2010b). Moderate contusion injuries (75 kDynes) were performed using the Infinite Horizon impactor device (Precision Systems and Instrumentation).…”

Section: Methodsmentioning

confidence: 99%

“…At 0,3,4,5,7,14,28, or 56 d after contusive SCI (n ϭ 5 per group) and at 3 or 14 d after dorsal hemisection (n ϭ 3 per group), mice were perfused transcardially with 4% PFA. Brains and spinal cords were harvested and prepared for immunohistochemistry as previously described (Lee et al, 2010a). Serial sagittal cryosections (10 m) of the injury site were immunostained for ␣-smooth muscle actin (␣SMA)-Cy3 (Sigma), CD11b (Invitrogen), CD13 (Abcam), CD45 (eBioscience), F4/80 (AbD Serotec), fibronectin (Millipore), Glut1 (Millipore), GFAP (Invitrogen), GFP (Abcam), laminin (Sigma), nestin (Aves Laboratories), NG2 (Millipore), Olig2 (Millipore), PDGFR-␤ (Abcam), PECAM/CD31 (BD Biosciences), RFP (Rockland), or 5-hydroxytryptamine (Immunostar) (Lee et al, 2010a).…”

Section: Methodsmentioning

confidence: 99%

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Perivascular Fibroblasts Form the Fibrotic Scar after Contusive Spinal Cord Injury

et al. 2013

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Injury to the CNS leads to formation of scar tissue, which is important in sealing the lesion and inhibiting axon regeneration. The fibrotic scar that comprises a dense extracellular matrix is thought to originate from meningeal cells surrounding the CNS. However, using transgenic mice, we demonstrate that perivascular collagen1␣1 cells are the main source of the cellular composition of the fibrotic scar after contusive spinal cord injury in which the dura remains intact. Using genetic lineage tracing, light sheet fluorescent microscopy, and antigenic profiling, we identify collagen1␣1 cells as perivascular fibroblasts that are distinct from pericytes. Our results identify collagen1␣1 cells as a novel source of the fibrotic scar after spinal cord injury and shift the focus from the meninges to the vasculature during scar formation.

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“…Rosa26-tdTomato reporter mice were kindly donated by Dr. Fan Wang, Duke University, Durham, NC (Lee et al, 2009). All mice had pure C57BL/6 genetic background.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Perivascular Fibroblasts Form the Fibrotic Scar after Contusive Spinal Cord Injury

et al. 2013

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“…Although there is no clear anatomical evidence that serotonergic axons effectively bridge the lesion site and extend into the caudal stump [41,42], infusion of the serotonin neurotoxin 5,7-dihydroxytryptamine moderately impairs the SM-216289-mediated recovery of slight hindlimb joint movement [42]. Genetic deletion of both signal transducing plexinA3 and plexinA4 fails to augment serotonergic axon regeneration [43]. Nevertheless, despite expression of receptors for class 3 semaphorins on intact and injured corticospinal neurons [26], neither small molecule inhibition nor genetic deletion of plexins (A3 and A4) resulted in any demonstrable regeneration of the corticospinal tract, suggesting that other factors may limit corticospinal axon plasticity after injury [41][42][43].…”

Section: Semaphorinsmentioning

confidence: 99%

Axon Guidance Molecules and Neural Circuit Remodeling After Spinal Cord Injury

Hollis

2016

Neurotherapeutics

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…once the development was ended, the founts of growth and regeneration of the axons and dendrites dried up irrevocably. Santiago Ramón y CajalCajal's neurotropic theory postulates that the complexity of the nervous system arises from the collaboration of neurotropic signals from neuronal and non-neuronal cells and that once development has ended, a paucity of neurotropic signals means that the pathways of the central nervous system are Bfixed, ended, immutable^. While the capacity for regeneration and plasticity of the central nervous system may not be quite as paltry as Cajal proposed, regeneration is severely limited in scope as there is no spontaneous regeneration of long-distance projections in mammals and therefore limited opportunity for functional recovery following spinal cord injury. It is not a far stretch from Cajal to hypothesize that reappropriation of the neurotropic programs of development may be an appropriate strategy for reconstitution of injured circuits. It has become clear, however, that a significant number of the molecular cues governing circuit development become re-active after injury and many assume roles that paradoxically obstruct the functional re-wiring of severed neural connections. Therefore, the problem to address is how individual neural circuits respond to specific molecular cues following injury, and what strategies will be necessary for instigating functional repair or remodeling of the injured spinal cord.

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Serotonin axons in the neocortex of the adult female mouse regrow after traumatic brain injury

Kajstura

Dougherty

Linden

2017

J of Neuroscience Research

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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.

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Combined Genetic Attenuation of Myelin and Semaphorin-Mediated Growth Inhibition Is Insufficient to Promote Serotonergic Axon Regeneration

Cited by 71 publications

References 37 publications

Perivascular Fibroblasts Form the Fibrotic Scar after Contusive Spinal Cord Injury

Perivascular Fibroblasts Form the Fibrotic Scar after Contusive Spinal Cord Injury

Axon Guidance Molecules and Neural Circuit Remodeling After Spinal Cord Injury

Serotonin axons in the neocortex of the adult female mouse regrow after traumatic brain injury

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