Relationship between circulating IGF-1 levels and traumatic brain injury-induced hippocampal damage and cognitive dysfunction in immature rats

Özdemir, Durgül; Baykara, Başak; Aksu, İlkay; Kıray, Müge; Şişman, Ali Rιza; Çetin, Ferihan; Dayı, Ayfer; Gürpınar, Tuğba; Uysal, Nazan; Arda, M. Nuri

doi:10.1016/j.neulet.2011.11.059

Cited by 47 publications

(28 citation statements)

References 34 publications

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“…41,42 In this study, a significant improvement in MWM performance in the ODN group was observed suggesting that antisense ODN ICV administration consequently improved chronic cognitive outcome of rats following TBI. We presumed that differences in Na v 1.3 expression level resulted from the variable secondary brain injury, which eventually led to differences in outcome, including degeneration during the acute stage and long-term cognitive behavior dysfunction.…”

supporting

confidence: 50%

Blockage of the Upregulation of Voltage-Gated Sodium Channel Na_v1.3 Improves Outcomes after Experimental Traumatic Brain Injury

Huang

Lin

et al. 2014

Journal of Neurotrauma

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Excessive active voltage-gated sodium channels are responsible for the cellular abnormalities associated with secondary brain injury following traumatic brain injury (TBI). We previously presented evidence that significant upregulation of Na v 1.3 expression occurs in the rat cortex at 2 h and 12 h post-TBI and is correlated with TBI severity. In our current study, we tested the hypothesis that blocking upregulation of Na v 1.3 expression in vivo in the acute stage post-TBI attenuates the secondary brain injury associated with TBI. We administered either antisense oligodeoxynucleotides (ODN) targeting Na v 1.3 or artificial cerebrospinal fluid (aCSF) at 2 h, 4 h, 6 h, and 8 h following TBI. Control sham animals received aCSF administration at the same time points. At 12 h post-TBI, Na v 1.3 messenger ribonucleic acid (mRNA) levels in bilateral hippocampi of the aCSF group were significantly elevated, compared with the sham and ODN groups ( p < 0.01). However, the Na v 1.3 mRNA levels in the uninjured contralateral hippocampus of the ODN group were significantly lowered, compared with the sham group ( p < 0.01). Treatment with antisense ODN significantly decreased the number of degenerating neurons in the ipsilateral hippocampal CA3 and hilar region ( p < 0.01). A set of left-to-right ratio value analyzed by magnetic resonance imaging T2 image on one day, three days, and seven days post-TBI showed marked edema in the ipsilateral hemisphere of the aCSF group, compared with that of the ODN group ( p < 0.05). The Morris water maze memory retention test showed that both the aCSF and ODN groups took longer to find a hidden platform, compared with the sham group ( p < 0.01). However, latency in the aCSF group was significantly higher than in the ODN group ( p < 0.05). Our in vivo Na v 1.3 inhibition studies suggest that therapeutic strategies to block upregulation of Na v 1.3 expression in the brain may improve outcomes following TBI.

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confidence: 50%

Blockage of the Upregulation of Voltage-Gated Sodium Channel Na_v1.3 Improves Outcomes after Experimental Traumatic Brain Injury

Huang

Lin

et al. 2014

Journal of Neurotrauma

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“…Although children with head trauma have better survival rates as compared with adults, the long-term sequelae and consequences are often more devastating in children due to their age and developmental level. Cognitive deficits are well-known sequelae of traumatic brain injury (TBI) that lead to long-term functional impairment and decrease in quality of life (11,26,27). In recent years, psychiatric disorders such as depression, anxiety disorders, and personality changes was seen following TBI (15,24,32,40).…”

Section: Introductionmentioning

confidence: 99%

“…Two brain structures such as cortex and the hippocampus is prominently affected in TBI (37). Hippocampus-related learning is well studied in immature rats with TBI (26,27); however there are few studies about experimental TBIinduced anxiety in rats. In Jones et al study, experimental TBI has been reported to trigger anxiety-like behavior in adult rats (14).…”

Section: Introductionmentioning

confidence: 99%

Anxiety caused by traumatic brain injury correlates to decreased prefrontal cortex vegf immunoreactivity and neuron density in immature rats

Baykara¹,

Çetin²,

Baykara³

et al. 2012

Turkish Neurosurgery

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AIm: Traumatic brain injury (TBI) may cause neuropsychiatric disorders such as anxiety disorder which has negative effects on cognitive functions and behavior. The aim of this study is to investigate the effects of TBI on anxiety and vascular endothelial growth factor (VEGF) immunoreactivity on the prefrontal cortex of immature rats, which is one of the anxiety-related regions of the brain in 7-day-old immature rats subjected to contusion injury. mATeRIAL and meTHods: Rats were divided into three groups: Control (n=7), Sham (n=7) and TBI (n=7). Anxiety levels were assessed with open field activity and elevated plus maze in postnatal 27 days. Prefrontal cortex damage related to TBI was examined by cresyl violet staining and VEGF immunostaining. Prefrontal cortex neuronal density was calculated. Serum corticosterone levels were determined. ResuLTs:The anxiety level in the TBI group was significantly greater than the control and sham groups. The prefrontal cortex VEGF immunostaining score and neuron density were decreased in the TBI group compared to control and sham group. Serum corticosterone levels were significantly increased in the TBI group. CoNCLusIoN:These results indicate that TBI decreases VEGF immunoreactivity in prefrontal cortex neurons and increases the anxiety levels of immature rats.

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“…Children have a higher survival rates compared to adults with head trauma; but, the long-term sequelae are often more devastating in children depending on the age and developmental period (1). The cognitive dysfunction is a common sequela of head trauma, which is not limited to severe injury but it can be seen in mild and moderate injury (4,17,31,32).…”

Section: Introductionmentioning

confidence: 99%

“…The immature brain is extremely vulnerable to TBI-induced apoptotic neurodegeneration (12,31,32). This developmental vulnerability period corresponds to the brain growth spurt period, the period that coincides with the first two postnatal weeks in the rats and the first 2 years in humans (5).…”

Section: Introductionmentioning

confidence: 99%

The combined treatment with progesterone and magnesium sulfate positively affects the traumatic brain injury in immature rats.

Uysal¹,

Baykara²,

Kıray³

et al. 2012

Turkish Neurosurgery

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AIm:It is well known that head trauma results in damage in hippocampal and cortical areas of the brain and impairs cognitive functions. The aim of this study is to explore the neuroprotective effect of combination therapy with magnesium sulphate (MgSO4) and progesterone in the 7-days-old rat pups subjected to contusion injury. mAterIAl and methOds: Progesterone (8 mg/kg) and MgSO4 (150 mg/kg) were injected intraperitoneally immediately after induction of traumatic brain injury. Half of groups were evaluated 24 hours later, the remaining animals 3 weeks after trauma or sham surgery. Anxiety levels were assessed with open field activity and elevated plus maze; learning and memory performance were evaluated with Morris Water maze in postnatal 27 days.results: Combined therapy with progesterone and magnesium sulfate significantly attenuated trauma-induced neuronal death, increased brain VEGF levels and improved spatial memory deficits that appear later in life. Brain VEGF levels were higher in rats that received combined therapy compared to rats that received either medication alone. Moreover, rats that received combined therapy had reduced hipocampus and prefrontal cortex apoptosis in the acute period.COnClusIOn: These results demonstrate that combination of drugs with different mechanisms of action may be preferred in the treatment of head trauma.KeywOrds: Traumatic brain injury, Immature rat, Spatial learning and memory, Apoptosis, VEGF, Magnesium sulfate, Progesterone ÖZ AmAÇ: Kafa travmasının hipokampal ve kortikal hasar ile kognitif fonksiyonlarda bozulmaya neden olduğu bilinmektedir. Bu çalışmanın amacı, magnezyum sülfat (MgSO4) ve progesteronun combine kullanımının kontüzyon hasarı oluşturulan 7 günlük sıçan beynindeki nöroprotektif etkilerini araştırmaktır. yÖntem ve GereÇler: Travmadan hemen sonra 8 mg/kg dozunda progesteron, 150 mg/kg dozunda MgSO4 intraperitoneal tek doz olarak verildi. Deney gruplarının yarısı travmadan 24 saat sonra, kalan yarısı ise 27 günlük olduklarında değerlendirildi. Anksiyete deneyleri açık alan ve yükseltilmiş + labirent test düzenekleri kullanılarak; öğrenme ve bellek performansı ise Morris su tankı aracılığı ile 27 günlükken değerlendirildi.BulGulAr: Kombine tedavinin beyin dokusunda VEGF'yi arttırarak travma ile oluşan nöronal ölümü azalttığı ve ileriki dönemde spasyal bellek bozukluğunu iyileştirdiği görüldü. VEGF seviyesinin kombine tedavide ilaçların tek başına kullanımına göre daha fazla arttığı bulundu. Ayrıca ilaç tedavisinin akut dönemde de VEGF seviyesini arttırarak apoptozis seviyesini azalttığı görüldü. sOnuÇ: Bu sonuçlar, farklı etki mekanizmasına sahip ilaçların kombine kullanımının kafa travması tedavisinde tercih edilebileceğini göstermektedir.

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Relationship between circulating IGF-1 levels and traumatic brain injury-induced hippocampal damage and cognitive dysfunction in immature rats

Cited by 47 publications

References 34 publications

Blockage of the Upregulation of Voltage-Gated Sodium Channel Na_v1.3 Improves Outcomes after Experimental Traumatic Brain Injury

Blockage of the Upregulation of Voltage-Gated Sodium Channel Na_v1.3 Improves Outcomes after Experimental Traumatic Brain Injury

Anxiety caused by traumatic brain injury correlates to decreased prefrontal cortex vegf immunoreactivity and neuron density in immature rats

The combined treatment with progesterone and magnesium sulfate positively affects the traumatic brain injury in immature rats.

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Relationship between circulating IGF-1 levels and traumatic brain injury-induced hippocampal damage and cognitive dysfunction in immature rats

Cited by 47 publications

References 34 publications

Blockage of the Upregulation of Voltage-Gated Sodium Channel Nav1.3 Improves Outcomes after Experimental Traumatic Brain Injury

Blockage of the Upregulation of Voltage-Gated Sodium Channel Nav1.3 Improves Outcomes after Experimental Traumatic Brain Injury

Anxiety caused by traumatic brain injury correlates to decreased prefrontal cortex vegf immunoreactivity and neuron density in immature rats

The combined treatment with progesterone and magnesium sulfate positively affects the traumatic brain injury in immature rats.

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Product

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Blockage of the Upregulation of Voltage-Gated Sodium Channel Na_v1.3 Improves Outcomes after Experimental Traumatic Brain Injury

Blockage of the Upregulation of Voltage-Gated Sodium Channel Na_v1.3 Improves Outcomes after Experimental Traumatic Brain Injury