Impact of Traumatic Brain Injury on Neurogenesis

Ngwenya, Laura B.; Danzer, Steve C.

doi:10.3389/fnins.2018.01014

Cited by 57 publications

(41 citation statements)

References 120 publications

(126 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This study demonstrates that maternal nicotine exposure in prepregnancy, pregnancy, and lactation stages impairs the behavioral performance, hippocampal neurogenesis, and microglial activation in the offspring. Our data support the view that maternal nicotine exposure produces an adverse effect on the offspring and is detrimental to the naturally occurring neurogenetic processes in the adult brain (Ngwenya and Danzer, 2018).…”

Section: Discussionsupporting

confidence: 86%

Maternal Nicotine Exposure During Gestation and Lactation Period Affects Behavior and Hippocampal Neurogenesis in Mouse Offspring

et al. 2020

View full text Add to dashboard Cite

Cigarette smoking or nicotine exposure during pregnancy is associated with numerous obstetrical, fetal, and developmental complications, as well as an increased risk of adverse health consequences in the adult offspring. In this study, we examined the effects of maternal nicotine exposure during perinatal and lactation stages on behavioral performance and hippocampal neurogenesis in the adolescent stage of offspring mice. Female C57BL/mice received nicotine in drinking water (200 mg/ml nicotine) or vehicle (1% saccharin) starting from 2 weeks premating until the offspring were weaned on postnatal day 20. Experiments started on postnatal day 35. Female offspring with maternal nicotine exposure presented an increase in anxiety-like behavior in an open-field test. BrdU assay revealed that nicotine offspring presented an increase in cell proliferation in hippocampal dentate gyrus, but the number of BrdU + cells was decreased in one week and further decreased in three weeks. The occurrence of disarray of DCX + cells increased in both male and female nicotine offspring. The density of microglial marker protein Iba1 was significantly increased in the nicotine offspring. Furthermore, the expression of microglia marker Iba1, the CX3CL1, CX3CR1, and downstream molecules PKA and pErK were significantly increased in the nicotine group. In summary, maternal nicotine exposure affects both hippocampal neurogenesis and microglial activity in the adolescent offspring.

show abstract

Section: Discussionsupporting

confidence: 86%

Maternal Nicotine Exposure During Gestation and Lactation Period Affects Behavior and Hippocampal Neurogenesis in Mouse Offspring

et al. 2020

View full text Add to dashboard Cite

show abstract

“…we have not ruled out the possibility that some of the EdU+ cells distant to the injury migrated 230 from areas closer to the wound. Similar effects at a distance from an injury have been observed 231 in rodent models of TBI (Urrea et al, 2007, Ngwenya andDanzer, 2018).…”

supporting

confidence: 69%

Regeneration in the adultDrosophilabrain

Crocker¹,

Marischuk²,

Rimkus³

et al. 2020

Preprint

View full text Add to dashboard Cite

Understanding the molecular and cellular mechanisms underlying neurogenesis after injury is crucial for developing tools for brain repair. We have established an adult Drosophila melanogaster model for investigating regeneration after central brain injury. Within 24 hours after Penetrating Traumatic Brain Injury (PTBI) to the central brain, we observe a significant increase in the number of proliferating cells. Between one- and two-weeks post-injury, we detect the generation of new neurons and glia and the formation of new axon tracts that target appropriate brain regions, suggesting there could be functional regeneration. Consistent with functional regeneration, locomotion abnormalities observed shortly after PTBI are largely reversed within 2 weeks of injury. Further, we find that cells surrounding the injury site upregulate neuroblast genes, such as asense and deadpan, and demonstrate that these cells give rise to the new neurons and glia. Taken together, our data support the hypothesis that young, adult Drosophila brains are capable of neuronal repair after central brain injury. We anticipate that our model will facilitate the dissection of the mechanisms of neural regeneration and anticipate that these processes will have relevance to humans.

show abstract

“…This latter phenomenon of granule cell-to-granule cell connectivity has been termed a recurrent excitatory circuitry [79,90]. This aberrant circuitry produces excitatory drive that can both promote and facilitate the spread of seizure activity [91,92], and more recent studies further support the role of this aberrant circuitry in epileptogenesis [93][94][95], including the involvement of injuryinduced atypical astrocytes [96]. Interestingly, a study also showed that during pilocarpine-induced epileptogenesis, the radial glial-like processes in the dentate gyrus upregulate the expression of CCR2.…”

Section: Astrocytes and Pte: Support Cell Inflammatory Mediator Ormentioning

confidence: 98%

Neuroinflammatory mechanisms of post-traumatic epilepsy

Mukherjee

Arisi

Mims

et al. 2020

J Neuroinflammation

View full text Add to dashboard Cite

Background: Traumatic brain injury (TBI) occurs in as many as 64-74 million people worldwide each year and often results in one or more post-traumatic syndromes, including depression, cognitive, emotional, and behavioral deficits. TBI can also increase seizure susceptibility, as well as increase the incidence of epilepsy, a phenomenon known as post-traumatic epilepsy (PTE). Injury type and severity appear to partially predict PTE susceptibility. However, a complete mechanistic understanding of risk factors for PTE is incomplete. Main body: From the earliest days of modern neuroscience, to the present day, accumulating evidence supports a significant role for neuroinflammation in the post-traumatic epileptogenic progression. Notably, substantial evidence indicates a role for astrocytes, microglia, chemokines, and cytokines in PTE progression. Although each of these mechanistic components is discussed in separate sections, it is highly likely that it is the totality of cellular and neuroinflammatory interactions that ultimately contribute to the epileptogenic progression following TBI. Conclusion: This comprehensive review focuses on the neuroinflammatory milieu and explores putative mechanisms involved in the epileptogenic progression from TBI to increased seizure-susceptibility and the development of PTE.

show abstract

Impact of Traumatic Brain Injury on Neurogenesis

Cited by 57 publications

References 120 publications

Maternal Nicotine Exposure During Gestation and Lactation Period Affects Behavior and Hippocampal Neurogenesis in Mouse Offspring

Maternal Nicotine Exposure During Gestation and Lactation Period Affects Behavior and Hippocampal Neurogenesis in Mouse Offspring

Regeneration in the adultDrosophilabrain

Neuroinflammatory mechanisms of post-traumatic epilepsy

Contact Info

Product

Resources

About