Erythropoietin improves place learning in fimbria–fornix-transected rats and modifies the search pattern of normal rats

Mogensen, Jesper; Sørensen, Thomas Alrik; Lind, Christopher Trier; Olsen, Niels Vidiendal; Springborg, Jacob Bertram; Malá, Hana

doi:10.1016/j.pbb.2003.11.017

Cited by 49 publications

(33 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In this regard, it has been demonstrated that rat pups given rHuEPO had a significantly better performance in the Morris water maze test compared with untreated animals (Kumral et al, 2004). Others subjected rats to bilateral transection of the fimbria-fornix and rHuEPO treatment allowed a better posttraumatic functional recovery (Mogensen et al, 2004). We have previously demonstrated that rHuEPO prevented cognition impairment in a gerbil transient brain ischemia model (Catania et al, 2002) and neurological dysfunction following experimental subarachnoid hemorrhage in rabbits (Grasso et al, 2002a).…”

Section: Discussionmentioning

confidence: 97%

Neuroprotection by erythropoietin administration after experimental traumatic brain injury

et al. 2007

View full text Add to dashboard Cite

A large body of evidence indicates that the hormone erythropoietin (EPO) exerts beneficial effects in the central nervous system (CNS). To date, EPO's effect has been assessed in several experimental models of brain and spinal cord injury. This study was conducted to validate whether treatment with recombinant human EPO (rHuEPO) would limit the extent of injury following experimental TBI. Experimental TBI was induced in rats by a cryogenic injury model. rHuEPO or placebo was injected intraperitoneally immediately after the injury and then every 8 h until 2 or 14 days. Forty-eight hours after injury brain water content, an indicator of brain edema, was measured with the wet-dry method and blood-brain barrier (BBB) breakdown was evaluated by assay of Evans blue extravasation. Furthermore, extent of cerebral damage was assessed. Administration of rHuEPO markedly improved recovery from motor dysfunction compared with placebo group (P < 0.05). Brain edema was significantly reduced in the cortex of the EPO-treated group relative to that in the placebo-treated group (80.6 ± 0.3% versus 91.8% ± 0.8% respectively, P < 0.05). BBB breakdown was significantly lower in EPO-treated group than in the placebo-treated group (66.2 ± 18.7 μg/g versus 181.3 ± 21 μg/g, respectively, P < 0.05). EPO treatment reduced injury volume significantly compared with placebo group (17.4 ± 5.4 mm3 versus 37.1 ± 5.3 mm3, P < 0.05). EPO, administered in its recombinant form, affords significant neuroprotection in experimental TBI model and may hold promise for future clinical applications.

show abstract

Section: Discussionmentioning

confidence: 97%

Neuroprotection by erythropoietin administration after experimental traumatic brain injury

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Subsequently, however, it turned out that EPO possesses a strong therapeutic potential even in TBI -including the ability to reduce posttraumatic cognitive impairments and support the cognitive rehabilitative processes (e.g. Lu et al, 2005;Malá et al, 2005Malá et al, , 2007Mogensen et al, 2004bMogensen et al, , 2008aMogensen et al, , 2008bWang et al, 2006). The degree to which such therapeutic effects are mediated via stimulation of BDNF remains unknown, but it is obvious that further research is needed in order to clarify some of the intricacies of the therapeutic use of EPO.…”

Section: Supporting the Posttraumatic Rehabilitative Processmentioning

confidence: 99%

Cognitive Recovery and Rehabilitation After Brain Injury: Mechanisms, Challenges and Support

Mogensen¹

2012

Brain Injury - Functional Aspects, Rehabilitation and Prevention

Self Cite

View full text Add to dashboard Cite

“…In addition, it could explain the effects of EPO in reducing seizure severity 10 as well as reported effects on learning and memory. 57 Other indirect effects of EPO that reduce neuronal injury have also been delineated. For example, EPO treatment increases astrocyte production of glutathione peroxidase and in this manner ameliorates neuronal damage caused by excitotoxins.…”

Section: Epo Signaling In Nervous System Cellsmentioning

confidence: 99%

Erythropoietin as an antiapoptotic, tissue-protective cytokine

Ghezzi

Brines²

2004

Cell Death Differ

307

238

View full text Add to dashboard Cite

Erythropoietin (EPO) increases the number of circulating erythrocytes primarily by preventing apoptosis of erythroid progenitors. In addition to this proerythroid action, results of recent studies show that systemically administered EPO is protective in vivo, in several animal models of neuronal injury. In vitro, EPO prevents neuronal apoptosis induced by a variety of stimuli. This review summarizes the neuroprotective actions of EPO and discusses the underlying mechanisms in terms of signal transduction pathways involved. The understanding of these mechanisms will help differentiate the neuroprotective actions of EPO from its role in the bone marrow.

show abstract

Erythropoietin improves place learning in fimbria–fornix-transected rats and modifies the search pattern of normal rats

Cited by 49 publications

References 55 publications

Neuroprotection by erythropoietin administration after experimental traumatic brain injury

Neuroprotection by erythropoietin administration after experimental traumatic brain injury

Cognitive Recovery and Rehabilitation After Brain Injury: Mechanisms, Challenges and Support

Erythropoietin as an antiapoptotic, tissue-protective cytokine

Contact Info

Product

Resources

About