Posttraumatic mossy fiber sprouting is related to the degree of cortical damage in three mouse strains

Hunt, Reid; Haselhorst, Laura A.; Schoch, Kathleen M.; Bach, Eva C.; Rios-Pilier, Jennifer; Saatman, Kathryn E.; Smith, Bret N.

doi:10.1016/j.eplepsyres.2011.10.011

Cited by 28 publications

(40 citation statements)

References 19 publications

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“…Our results support previously published observations that demonstrated robust mossy fiber sprouting in the IML of the hippocampus following FPI and/or CCI (Golarai et al, 2001;Santhakumar et al, 2001;Hunt et al, 2009Hunt et al, , 2010. Several important factors might affect mossy fiber sprouting and seizure incidence after brain injury, such as impact parameters, injury location, animal age, and rodent species (Hunt et al, 2012). In addition, excitatory drive to surviving hilar GABAergic interneurons after CCI may be enhanced by convergent input from both pyramidal and granule cells resulting in network destabilization (Hunt et al, 2011).…”

Section: Brain Pathologysupporting

confidence: 88%

Posttraumatic seizures and epilepsy in adult rats after controlled cortical impact

et al. 2015

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Section: Brain Pathologysupporting

confidence: 88%

Posttraumatic seizures and epilepsy in adult rats after controlled cortical impact

et al. 2015

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“…A diffusion tensor imaging study conducted on a FPI rat model at 6 -12 mo postinjury showed that injured animals had thicker mossy fibers, decreased myelinated axons within the CA3 region and increased mossy fiber sprouting within the dentate gyrus (42). However, these processes abort without becoming functional (43)(44)(45). Since a role of PLs in axonal growth and sprouting is suggested by studies showing synthesis of PC, PE, and SM within axons (46,47), PL changes after injury in the hippocampi may be associated with self-reparative processes.…”

Section: Discussionmentioning

confidence: 99%

Lipidomic analyses identify injury‐specific phospholipid changes 3 mo after traumatic brain injury

et al. 2014

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Phospholipid (PL) abnormalities are observed in the cerebrospinal fluid of patients with traumatic brain injury (TBI), suggesting their role in TBI pathology. Therefore, PL levels were examined in a TBI mouse model that received 1.8 mm deep controlled cortical impact injury or craniectomy only (control). The rotarod and Barnes maze acquisition and probe tests were performed within 2 wk after injury, with another probe test performed 3 mo postinjury. Liquid chromatography/mass spectrometry analyses were performed on lipid extracts from several brain regions and plasma from injured and control mice collected at 3 mo postinjury. Compared to controls, injured mice with sensorimotor and learning deficits had decreased levels of cortical and cerebellar phosphatidylcholine (PC) and phosphatidylethanolamine (PE) levels, while hippocampal PC, sphingomyelin and PE levels were elevated. Ether PE levels were lower in the cortices and plasma of injured animals. Polyunsaturated fatty acid-containing PC and PE species, particularly ratios of docosahexaenoic acid (DHA) to arachidonic acid, were lower in the hippocampi and cortices and plasma of injured mice. Given the importance of DHA in maintaining neuronal function and resolving inflammation and of peroxisomes in synthesis of ether PLs, normalizing these PLs may be a useful strategy for treating the chronic pathology of TBI.-Abdullah, L., Evans, J. E., Ferguson, S., Mouzon, B., Montague, H., Reed, J., Crynen, G., Emmerich, T., Crocker, M., Pelot, R., Mullan, M., Crawford, F. Lipidomic analyses identify injury-specific phospholipid changes 3 months after traumatic brain injury. FASEB J. 28, 5311-5321 (2014). www.fasebj.org Key Words: controlled cortical impact ⅐ mass spectrometry ⅐ phosphatidylcholine ⅐ phosphatidylethanolamine ⅐ phosphatidylinositol ⅐ sphingomyelin Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in the United States among adults from both the civilian and military populations. Due to the improvements made in military body armor and combat helmets over the past 2 decades, the rate of severe TBI associated with Iraq and Afghanistan deployments has decreased to 1% of the total TBI sustained by military personnel, a rate that is lower than those reported for previous deployments (1-3). Estimates from the U.S. Centers for Disease Control and Prevention suggest that severe TBI remains an important issue in the civilian population. In 2010, 2.5 million admissions to emergency departments were due to TBI (4) contributing to about a third of injury related deaths in the United States. The annual U.S. costs associated with TBI are estimated to be $75 billion, largely attributed to medical care, loss of productivity, and long-term disability (5). Although mild TBI occurs more frequently than severe TBI, the latter has the largest adverse effect on the activities of daily living of injured individuals and accounts for 90% of the total TBI-related medical costs (5). The primary injury is caused by the immediate force of the trauma a...

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“…A variable degree of mossy fiber sprouting and synaptic reorganization in the dentate gyrus, as well as axon sprouting onto hilar interneurons has also been observed in concert with development of PTE and other forms of acquired epilepsy (19,22,26,29,35,36). Mossy fiber sprouting is localized to areas near the injury epicenter after focal injury (29) and is less severe and sparser after TBI than, for example, in chemoconvulsant models of TLE, but its presence, however limited, is a consistent feature of both models. Other cellular outcomes identified in both TLE and PTE models include an increase in postinjury granule cell progenitor proliferation and a reorganization of GABA A receptors in granule cells (33,(37)(38)(39)(40).…”

Section: Convergence Of Cellular Changes In Pte and Tle Modelsmentioning

confidence: 99%

“…The injury occasionally results in early seizures (<24 hours) (22,25), and spontaneous convulsive seizures develop in 40 to 50% of mice within approximately 8 weeks after severe injury (22,23,(26)(27)(28)) and 9 to 20% of mice after more moderate injuries (18,22,26). Like other murine epilepsy models, mouse strain may also influence seizure phenotype and the incidence of PTE (18,29). Seizures after CCI are similar to spontaneous behavioral and electrographic seizures that have been described in rats after LFPI (19) and in models of acquired TLE (30,31).…”

Section: Rodent Modelsmentioning

confidence: 99%

How and Why Study Posttraumatic Epileptogenesis in Animal Models?

Smith

2016

Epilepsy Curr

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Over 2 million people are treated medically each year in the United States after sustaining a traumatic brain injury (TBI) (1), and posttraumatic epilepsy (PTE), which is often intractable to medical treatment, is a common long-term consequence of TBI. Epilepsy affects 1% to 2% of the population (2), but the overall incidence of epilepsy after moderate-to-severe closedhead injury is 7% to 39% and is over 50% after penetrating injury (3)(4)(5). Approximately 20% of all symptomatic epilepsies result from TBI (6), making PTE one of the most prevalent types of epilepsy. Although a number of seizure types can develop after brain trauma, PTE manifests as temporal lobe epilepsy (TLE, either neocortical or mesial) in 35 to 62% of trauma patients (7-9). As with other forms of acquired epilepsy, spontaneous recurrent seizures associated with PTE develop with a latency ranging from weeks to many years after the initial injury. This seizure-free period after TBI is thought to represent the period of epileptogenesis, during which the brain undergoes physiological, anatomic, cellular, and molecular changes that lead to a state of chronically increased seizure susceptibility. In principle, this delay between the TBI and development of PTE also represents a window of opportunity during which strategies might be employed to inhibit the reactive plasticity in the brain that leads to PTE, but no antiepileptogenic therapies have been successfully developed to date. This review focuses on key pathophysiological changes in the brain associated with posttraumatic epileptogenesis, animal models used to study those changes, and efforts to identify predictive biomarkers of PTE and to employ candidate treatments to prevent PTE.TBI results in acute cell death, axon injury, vascular damage, and accompanying excitotoxicity shortly after injury. Secondary damage, occurring within days of the primary injury, including or resulting from hypoxia/ischemia, delayed necrotic and apoptotic cell death, oxidative stress, gliosis, edema, blood brain barrier disruption, and inflammation may exacerbate initial damage. Putative homeostatic repair mechanisms, including angiogenesis, synaptic reorganization, and neurogenesis can engage over time and are hypothesized to compensate for functional loss resulting from the initial injury; they are also associated with PTE. By their very nature, brain injuries are highly variable across patients, and this heterogeneity is reflected in a wide variety of epileptogenic responses to injury. Injury severity and location, the presence of seizures shortly after injury, intracranial hemorrhage, cortical contusion, the level of postinjury consciousness impairment, age, and sex have all been implicated as potential factors associated with increased risk of developing PTE after brain trauma (4, 5, 10). Many of the cellular events that occur after TBI also occur after insults used to induce epilepsy in animal models, and rodent models of PTE have been developed with the goal of identifying those factors associated with the e...

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Posttraumatic mossy fiber sprouting is related to the degree of cortical damage in three mouse strains

Cited by 28 publications

References 19 publications

Posttraumatic seizures and epilepsy in adult rats after controlled cortical impact

Posttraumatic seizures and epilepsy in adult rats after controlled cortical impact

Lipidomic analyses identify injury‐specific phospholipid changes 3 mo after traumatic brain injury

How and Why Study Posttraumatic Epileptogenesis in Animal Models?

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