Abstract
Background Tumor necrosis factor (TNF)-α has been suggested to play both a deleterious and beneficial role in neurobehavioral dysfunction and recovery following traumatic brain injury (TBI). The goal of this study was to evaluate the specific role of tumor necrosis factor (TNF) receptors p55 and p75 in mediating cognitive outcome following controlled cortical impact (CCI) brain injury by comparing post-traumatic cognitive function in mice with genetically engineered deletion of the gene for either p55 (-/-) or p75 (-/-) receptors. Method Male C57Bl/6 mice (WT, n=29), and mice genetically engineered to delete p55 TNF (p55 (-/-), n=8) or p75 TNF (p75 (-/-), n=23) receptors were used. They were anesthetized with intraperitoneal (i.p.) administration of sodium pentobarbital (65 mg/kg) and subjected to CCI brain injury of moderate severity. Sham-injured control mice were anesthetized and surgically prepared similarly but they received no impact. Assessment of mRNA expression of inflammatory, proapoptotic and antiapoptotic genes was done by real time-polymerase chain reaction (RT-PCR). Cognitive outcome was evaluated at 4 weeks postinjury using the Morris water maze (MWM). Findings mRNA expression of inflammatory, proapoptotic and antiapoptotic genes prior to TBI did not reveal any baseline difference between p55 and p75 (-/-) mice. WT mice showed greater baseline expression of inflammatory genes. The learning ability of p55 (-/-) brain-injured mice was significantly better than that observed in p75 (-/-) brain-injured mice (p
| Original language | English |
|---|---|
| Title of host publication | Acta Neurochirurgica, Supplementum |
| Pages | 409-413 |
| Number of pages | 5 |
| Edition | 102 |
| DOIs | |
| Publication status | Published - 2008 |
Publication series
| Name | Acta Neurochirurgica, Supplementum |
|---|---|
| Number | 102 |
| ISSN (Print) | 00651419 |
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Keywords
- Apoptosis
- Inflammation
- TNF-α
- Traumatic brain injury
ASJC Scopus subject areas
- Clinical Neurology
- Surgery
Cite this
Effect of traumatic brain injury on cognitive function in mice lacking p55 and p75 tumor necrosis factor receptors. / Longhi, L.; Ortolano, F.; Zanier, E. R.; Perego, C.; Stocchetti, N.; De Simoni, M. G.
Acta Neurochirurgica, Supplementum. 102. ed. 2008. p. 409-413 (Acta Neurochirurgica, Supplementum; No. 102).Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - Effect of traumatic brain injury on cognitive function in mice lacking p55 and p75 tumor necrosis factor receptors
AU - Longhi, L.
AU - Ortolano, F.
AU - Zanier, E. R.
AU - Perego, C.
AU - Stocchetti, N.
AU - De Simoni, M. G.
PY - 2008
Y1 - 2008
N2 - Background Tumor necrosis factor (TNF)-α has been suggested to play both a deleterious and beneficial role in neurobehavioral dysfunction and recovery following traumatic brain injury (TBI). The goal of this study was to evaluate the specific role of tumor necrosis factor (TNF) receptors p55 and p75 in mediating cognitive outcome following controlled cortical impact (CCI) brain injury by comparing post-traumatic cognitive function in mice with genetically engineered deletion of the gene for either p55 (-/-) or p75 (-/-) receptors. Method Male C57Bl/6 mice (WT, n=29), and mice genetically engineered to delete p55 TNF (p55 (-/-), n=8) or p75 TNF (p75 (-/-), n=23) receptors were used. They were anesthetized with intraperitoneal (i.p.) administration of sodium pentobarbital (65 mg/kg) and subjected to CCI brain injury of moderate severity. Sham-injured control mice were anesthetized and surgically prepared similarly but they received no impact. Assessment of mRNA expression of inflammatory, proapoptotic and antiapoptotic genes was done by real time-polymerase chain reaction (RT-PCR). Cognitive outcome was evaluated at 4 weeks postinjury using the Morris water maze (MWM). Findings mRNA expression of inflammatory, proapoptotic and antiapoptotic genes prior to TBI did not reveal any baseline difference between p55 and p75 (-/-) mice. WT mice showed greater baseline expression of inflammatory genes. The learning ability of p55 (-/-) brain-injured mice was significantly better than that observed in p75 (-/-) brain-injured mice (p
AB - Background Tumor necrosis factor (TNF)-α has been suggested to play both a deleterious and beneficial role in neurobehavioral dysfunction and recovery following traumatic brain injury (TBI). The goal of this study was to evaluate the specific role of tumor necrosis factor (TNF) receptors p55 and p75 in mediating cognitive outcome following controlled cortical impact (CCI) brain injury by comparing post-traumatic cognitive function in mice with genetically engineered deletion of the gene for either p55 (-/-) or p75 (-/-) receptors. Method Male C57Bl/6 mice (WT, n=29), and mice genetically engineered to delete p55 TNF (p55 (-/-), n=8) or p75 TNF (p75 (-/-), n=23) receptors were used. They were anesthetized with intraperitoneal (i.p.) administration of sodium pentobarbital (65 mg/kg) and subjected to CCI brain injury of moderate severity. Sham-injured control mice were anesthetized and surgically prepared similarly but they received no impact. Assessment of mRNA expression of inflammatory, proapoptotic and antiapoptotic genes was done by real time-polymerase chain reaction (RT-PCR). Cognitive outcome was evaluated at 4 weeks postinjury using the Morris water maze (MWM). Findings mRNA expression of inflammatory, proapoptotic and antiapoptotic genes prior to TBI did not reveal any baseline difference between p55 and p75 (-/-) mice. WT mice showed greater baseline expression of inflammatory genes. The learning ability of p55 (-/-) brain-injured mice was significantly better than that observed in p75 (-/-) brain-injured mice (p
KW - Apoptosis
KW - Inflammation
KW - TNF-α
KW - Traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=66649093643&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=66649093643&partnerID=8YFLogxK
U2 - 10.1007/978-3-211-85578-2-80
DO - 10.1007/978-3-211-85578-2-80
M3 - Chapter
C2 - 19388357
AN - SCOPUS:66649093643
SN - 9783211855775
T3 - Acta Neurochirurgica, Supplementum
SP - 409
EP - 413
BT - Acta Neurochirurgica, Supplementum
ER -