Anatomical integration of newly generated dentate granule neurons following traumatic brain injury in adult rats and its association to cognitive recovery

Sun, Dong; McGinn, Melissa J.; Zhou, Zheng; Harvey, H. B.; Bullock, M. Ross; Colello, Raymond J.

doi:10.1016/j.expneurol.2006.11.005

Cited by 169 publications

(173 citation statements)

References 39 publications

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“…42,46,47,74 However, the literature is far from agreement on how the hippocampus is affected by trauma. In the current study, our finding of an unaltered number of migrating neuroblasts in the hippocampus of children following TBI is similar to the results of Chirumamilla and colleagues, 11 who did not observe increased neurogenesis in the hippocampus of adult rats 48 hours after fluid percussion injury.…”

Section: Discussionmentioning

confidence: 99%

Maturation-dependent response of neurogenesis after traumatic brain injury in children

Taylor

Smith²,

Harris

et al. 2013

PED

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Object Traumatic brain injury (TBI) is the leading cause of acquired disability in children, yet innate repair mechanisms are incompletely understood. Given data from animal studies documenting neurogenesis in response to trauma and other insults, the authors investigated whether similar responses could be found in children of different ages after TBI. Methods Immunohistochemistry was used to label doublecortin (DCX), a protein expressed by immature migrating neuroblasts (newborn neurons), in specimens from patients ranging in age from 3 weeks to 10 years who had died either after TBI or from other causes. Doublecortin-positive (DCX+) cells were examined in the subventricular zone (SVZ) and periventricular white matter (PWM) and were quantified within the granule cell layer (GCL) and subgranular zone (SGZ) of the dentate gyrus to determine if age and/or injury affect the number of DCX+ cells in these regions. Results The DCX+ cells decreased in the SVZ as patient age increased and were found in abundance around a focal subacute infarct in a 1-month-old non-TBI patient, but were scarce in all other patients regardless of age or history of trauma. The DCX+ cells in the PWM and dentate gyrus demonstrated a migratory morphology and did not co-localize with markers for astrocytes, microglia, or macrophages. In addition, there were significantly more DCX+ cells in the GCL and SGZ of the dentate gyrus in children younger than 1 year old than in older children. The density of immature migrating neuroblasts in infants (under 1 year of age) was significantly greater than in young children (2–6 years of age, p = 0.006) and older children (7–10 years of age, p = 0.007). Conclusions The main variable influencing the number of migrating neuroblasts observed in the SVZ, PWM, and hippocampus was patient age. Trauma had no discernible effect on the number of migrating neuroblasts in this cohort of patients in whom death typically occurred within hours to days after TBI.

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Section: Discussionmentioning

confidence: 99%

Maturation-dependent response of neurogenesis after traumatic brain injury in children

Taylor

Smith²,

Harris

et al. 2013

PED

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“…Increased, 22,29,30 unchanged, 23,32,34 and decreased 28 neurogenesis have all been reported post-TBI. However, these studies have been done in different TBI models: fluid percussion injury (FPI), 23,27,29,30 controlled cortical injury (CCI), 28,32 cortical contusion, 22 and impact-acceleration. 34 Because different models represent different aspects of human pathological characteristics, 35 they may induce different severities of TBI, although most studies were conducted in moderate levels in specific models.…”

Section: Introductionmentioning

confidence: 99%

“…Studies have shown that TBI promotes NSC proliferation, [22][23][24][25][26][27][28][29][30][31][32][33][34] while data for elucidating neurogenesis after TBI are contradictory. Increased, 22,29,30 unchanged, 23,32,34 and decreased 28 neurogenesis have all been reported post-TBI.…”

Section: Introductionmentioning

confidence: 99%

Traumatic Brain Injury Severity Affects Neurogenesis in Adult Mouse Hippocampus

Wang

Gao

Michalski

et al. 2016

Journal of Neurotrauma

110

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Traumatic brain injury (TBI) has been proven to enhance neural stem cell (NSC) proliferation in the hippocampal dentate gyrus. However, various groups have reported contradictory results on whether TBI increases neurogenesis, partially due to a wide range in the severities of injuries seen with different TBI models. To address whether the severity of TBI affects neurogenesis in the injured brain, we assessed neurogenesis in mouse brains receiving different severities of controlled cortical impact (CCI) with the same injury device. The mice were subjected to mild, moderate, or severe TBI by a CCI device. The effects of TBI severity on neurogenesis were evaluated at three stages: NSC proliferation, immature neurons, and newly-generated mature neurons. The results showed that mild TBI did not affect neurogenesis at any of the three stages. Moderate TBI promoted NSC proliferation without increasing neurogenesis. Severe TBI increased neurogenesis at all three stages. Our data suggest that the severity of injury affects adult neurogenesis in the hippocampus, and thus it may partially explain the inconsistent results of different groups regarding neurogenesis following TBI. Further understanding the mechanism of TBI-induced neurogenesis may provide a potential approach for using endogenous NSCs to protect against neuronal loss after trauma.

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“…The examples include considerable increases in the dentate neurogenesis observed in the young brain after ischemia, stroke or hypoxic injury (Liu et al ., 1998;Jin et al ., 2001Jin et al ., , 2004 and acute seizures or status epilepticus induced through excitotoxins or cholinomimetic chemicals (Bengzon et al ., 1997;Parent et al ., 1997Parent et al ., , 2006Gray & Sundstrom, 1998;Hattiangady et al ., 2004;Gong et al ., 2007). Although the precise benefits or adverse effects of increased neurogenesis after brain injury are still being studied (Parent, 2003;Jessberger et al ., 2007;, it is generally believed that this plasticity is useful for reducing impairments in cognitive functions after brain injury (Kleindienst et al ., 2005;Sun et al ., 2007). However, it is unknown whether aging alters the response of NSCs in the DG to brain injury, as most studies on changes in dentate neurogenesis following injury were performed using young animals.…”

Section: Introductionmentioning

confidence: 99%

Plasticity of hippocampal stem/progenitor cells to enhance neurogenesis in response to kainate‐induced injury is lost by middle age

2007

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SummaryA remarkable up-regulation of neurogenesis through increased proliferation of neural stem/progenitor cells (NSCs) is a well-known plasticity displayed by the young dentate gyrus (DG) following brain injury. To ascertain whether this plasticity is preserved during aging, we quantified DG neurogenesis in the young adult, middleaged and aged F344 rats after kainic acid induced hippocampal injury. Measurement of new cells that are added to the dentate granule cell layer (GCL) between post-injury days 4 and 15 using 5′ ′ ′ ′ -bromodeoxyuridine labeling revealed an increased addition of new cells in the young DG but not in the middle-aged and aged DG. Quantification of newly born neurons using doublecortin immunostaining also demonstrated a similar trend. Furthermore, the extent of ectopic migration of new neurons into the dentate hilus was dramatically increased in the young DG but was unaltered in the middle-aged and aged DG. However, there was no change in neuronal fate-choice decision of newly born cells following injury in all age groups. Similarly, comparable fractions of new cells that are added to the GCL after injury exhibited 5-month survival and expressed the mature neuronal marker NeuN, regardless of age or injury at the time of their birth. Thus, hippocampal injury does not adequately stimulate NSCs in the middle-aged and aged DG, resulting in no changes in neurogenesis after injury. Interestingly, rates of both neuronal fate-choice decision and long-term survival of newly born cells remain stable with injury in all age groups. These results underscore that the ability of the DG to increase neurogenesis after injury is lost as early as middle age.

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Anatomical integration of newly generated dentate granule neurons following traumatic brain injury in adult rats and its association to cognitive recovery

Cited by 169 publications

References 39 publications

Maturation-dependent response of neurogenesis after traumatic brain injury in children

Maturation-dependent response of neurogenesis after traumatic brain injury in children

Traumatic Brain Injury Severity Affects Neurogenesis in Adult Mouse Hippocampus

Plasticity of hippocampal stem/progenitor cells to enhance neurogenesis in response to kainate‐induced injury is lost by middle age

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