Enhancement in cognitive function recovery by granulocyte-colony stimulating factor in a rodent model of traumatic brain injury
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Authors
Sikoglu, Elif M.Heffernan, Meghan E.
Tam, Kelly
Sicard, Kenneth M.
Bratane, Bernt T.
Quan, Meina
Fisher, Marc
King, Jean A.
Document Type
Journal ArticlePublication Date
2014-02-01Keywords
AnimalsArea Under Curve
Brain Injuries
Cognition Disorders
Disease Models, Animal
Granulocyte Colony-Stimulating Factor
Male
Neuropsychological Tests
Rats
Rats, Wistar
Recovery of Function
Time Factors
Behavioral Neurobiology
Mental and Social Health
Nervous System Diseases
Neurology
Psychiatry
Psychiatry and Psychology
Metadata
Show full item recordAbstract
Traumatic brain injury (TBI) is characterized by neuronal damage and commonly, secondary cell death, leading to functional and neurological dysfunction. Despite the recent focus of TBI research on developing therapies, affective therapeutic strategies targeting neuronal death associated with TBI remain underexplored. This study explored the efficacy of granulocyte-colony stimulating factor (G-CSF) as an intervention for improving cognitive deficits commonly associated with TBI. Although G-CSF has been studied with histological techniques, to date, its effects on functional outcome remain unknown. To this end, we used a closed head injury (CHI) model in Wistar rats that were randomly assigned to one of four groups (untreated TBI, G-CSF treated TBI, G-CSF treated Control, Control). The treatment groups were administered subcutaneous injections of G-CSF 30 min (120 mug/kg) and 12 h (60 mug/kg) post-trauma. The Morris Water Maze test was used to measure any treatment-associated changes in cognitive deficits observed in TBI animals at days 2-6 post-injury. Our findings demonstrate a significant improvement in cognitive performance in the G-CSF treated TBI animals within a week of injury, compared to untreated TBI, indicative of immediate and beneficial effect of G-CSF on cognitive performance post CHI. Our model suggests that early G-CSF exposure may be a promising therapeutic approach in recovery of cognitive deficits due to TBI.Source
Behav Brain Res. 2014 Feb 1;259:354-6. doi: 10.1016/j.bbr.2013.11.008. Link to article on publisher's siteDOI
10.1016/j.bbr.2013.11.008Permanent Link to this Item
http://hdl.handle.net/20.500.14038/46157PubMed ID
24239694Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1016/j.bbr.2013.11.008