Gene expression alterations of neurotrophins, their receptors and prohormone convertases in a rat model of spinal cord contusion

Hajebrahimi, Zahra; Mowla, Seyed Javad; Movahedin, Mansureh; Tavallaei, Mahmood

doi:10.1016/j.neulet.2008.06.046

Cited by 31 publications

(20 citation statements)

References 26 publications

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“…In addition, In the present study, TrkC mRNA expression was found to be down-regulated in the earlier stage after injury (3-7 dpo), but up-regulated in the later stage after injury (14 dpo). This is somewhat different from a recent report by Hajebrahimi et al [14] who revealed that TrkC mRNA expression is continuously down-regulated and completely shut down in the injured cord up to 3 weeks after contusive injury. This discrepancy may be attributed to the differences in animal models and in the experiment methods [15] .…”

Section: Discussioncontrasting

confidence: 99%

Expression of tyrosine kinase receptor C in the segments of the spinal cord and the cerebral cortex after cord transection in adult rats

et al. 2011

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Section: Discussioncontrasting

confidence: 99%

Expression of tyrosine kinase receptor C in the segments of the spinal cord and the cerebral cortex after cord transection in adult rats

et al. 2011

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“…Moreover, other molecular changes associated with depression, such as decreased brain-derived neurotrophic factor (BDNF) levels and changes in glucocorticoid expression, are also observed in spinal tissue after injury. [65][66][67][68][69][70][71][72][73] Fumagalli and colleagues 74 also reported that SCI reduced hippocampal expression of BDNF messenger RNA levels for at least 7 days after injury, and elevations in serum corticosterone levels appear within 24 h after a mid-thoracic (T9) contusion injury persisting for at least 1 month after injury. 75,76 Whereas there is evidence that BDNF and corticosterone levels are modulated by cytokines, it is also possible that changes in the levels of BDNF and corticosterone after SCI affect psychological wellbeing through processes independent of proinflammatory cytokine expression.…”

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confidence: 98%

Assessment of Depression in a Rodent Model of Spinal Cord Injury

Luedtke

Bouchard

Woller

et al. 2014

Journal of Neurotrauma

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Despite an increased incidence of depression in patients after spinal cord injury (SCI), there is no animal model of depression after SCI. To address this, we used a battery of established tests to assess depression after a rodent contusion injury. Subjects were acclimated to the tasks, and baseline scores were collected before SCI. Testing was conducted on days 9-10 (acute) and 19-20 (chronic) postinjury. To categorize depression, subjects' scores on each behavioral measure were averaged across the acute and chronic stages of injury and subjected to a principal component analysis. This analysis revealed a two-component structure, which explained 72.2% of between-subjects variance. The data were then analyzed with a hierarchical cluster analysis, identifying two clusters that differed significantly on the sucrose preference, open field, social exploration, and burrowing tasks. One cluster (9 of 26 subjects) displayed characteristics of depression. Using these data, a discriminant function analysis was conducted to derive an equation that could classify subjects as ''depressed'' on days 9-10. The discriminant function was used in a second experiment examining whether the depression-like symptoms could be reversed with the antidepressant, fluoxetine. Fluoxetine significantly decreased immobility in the forced swim test (FST) in depressed subjects identified with the equation. Subjects that were depressed and treated with saline displayed significantly increased immobility on the FST, relative to not depressed, saline-treated controls. These initial experiments validate our tests of depression, generating a powerful model system for further understanding the relationships between molecular changes induced by SCI and the development of depression.

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“…16 Evidence from other studies suggests that p75NTR expression is enhanced post-injury. 6,8,17 Most of these studies investigated mRNA expression rather than protein expression with partial chronological resolution. The main function of p75NTR however, remains elusive.…”

Section: Discussionmentioning

confidence: 99%

“…5 In con-controversial, because this receptor can exert different effects depending on the cellular context, the type of ligand bound to it, and the presence or absence of Trk receptor. [6][7][8] P75NTR is initially expressed very early in embryogenesis in cells derived from all three germinal layers and becomes progressively restricted to specific cell populations such as CNS and peripheral nervous system. The p75NTR expression is induced after pathological conditions in a wide variety of cell types.…”

Section: Introductionmentioning

confidence: 99%

Messenger RNA expression patterns of p75 neurotrophin receptor and tropomyosin-receptor-kinase A following spinal cord injury

Montazeri

Esmaeili

Miroliaei

et al. 2013

The Journal of Spinal Cord Medicine

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Background: Induction of p75 neurotrophin receptor (p75NTR) could be one of the first steps that initiate apoptotic cascade after injury, or it may indicate regeneration responses undertaken by the injured system, possibly in collaboration with resident tropomyosin-receptor-kinase (Trk). Objective: To measure quantitative changes in messenger RNA (mRNA) expression levels of p75NTR, Trk A, and caspase-9 in rat's injured spinal cord (SCI). The reciprocal interaction between Trk and p75NTR signaling pathways can dictate cellular responses to neurotrophins. p75NTR can regulate Trk-dependent responses, but the role of Trk in regulating p75NTR-dependent signaling is not well documented. Design: Using real-time polymerase chain reaction, this study analyzed changes in the mRNA abundance of the mentioned genes at 6, 24, and 72 hours and 7 and 10 days after SCI in adult male rats. SCI was induced at T9 level by transsection. Results: Results show a complicated temporal and spatial pattern of alteration with different degrees and direction (up-or down-regulation) in p75NTR, Trk A, and caspase-9 mRNA expression levels after SCI. The greatest variation was seen in center regions following SCI. This study shows that alteration in p75NTR, Trk A, and caspase-9 expression starts as early as 6 hours after SCI. Alterations in p75NTR, Trk A, and caspase-9 expression within the spinal cord may play a key role in the apoptotic cell death. Conclusion: Results suggest that the role of p75NTR is to eliminate damaged cells by activating the apoptotic machinery, especially at the center of damage and during first week after injury.

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Gene expression alterations of neurotrophins, their receptors and prohormone convertases in a rat model of spinal cord contusion

Cited by 31 publications

References 26 publications

Expression of tyrosine kinase receptor C in the segments of the spinal cord and the cerebral cortex after cord transection in adult rats

Expression of tyrosine kinase receptor C in the segments of the spinal cord and the cerebral cortex after cord transection in adult rats

Assessment of Depression in a Rodent Model of Spinal Cord Injury

Messenger RNA expression patterns of p75 neurotrophin receptor and tropomyosin-receptor-kinase A following spinal cord injury

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