TY  - JOUR
A1  - Albert-Weißenberger, Christiane
A1  - Várrallyay, Csanád
A1  - Raslan, Furat
A1  - Kleinschnitz, Christoph
A1  - Sirén, Anna-Leena
T1  - An experimental protocol for mimicking pathomechanisms of traumatic brain injury in mice
N2  - Traumatic brain injury (TBI) is a result of an outside force causing immediate mechanical disruption of brain tissue and delayed pathogenic events. In order to examine injury processes associated with TBI, a number of rodent models to induce brain trauma have been described. However, none of these models covers the entire spectrum of events that might occur in TBI. Here we provide a thorough methodological description of a straightforward closed head weight drop mouse model to assess brain injuries close to the clinical conditions of human TBI.
KW  - Medizin
KW  - closed head injury
KW  - traumatic brain injury
KW  - neurobehavioural deficits
KW  - astrocyte
KW  - microglia
KW  - neurons
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-75368
ER  - 
TY  - JOUR
A1  - Michalski, D.
A1  - Heindl, M.
A1  - Kacza, J.
A1  - Laignel, F.
A1  - Küppers-Tiedt, L.
A1  - Schneider, D.
A1  - Grosche, J.
A1  - Boltze, J.
A1  - Löhr, M.
A1  - Hobohm, C.
A1  - Härtig, W.
T1  - Spatio-temporal course of macrophage-like cell accumulation after experimental embolic stroke depending on treatment with tissue plasminogen activator and its combination with hyperbaric oxygenation
JF  - European Journal of Histochemistry
N2  - Inflammation following ischaemic stroke attracts high priority in current research, particularly using human-like models and long-term observation periods considering translational aspects. The present study aimed on the spatio-temporal course of macrophage-like cell accumulation after experimental thromboembolic stroke and addressed microglial and astroglial reactions in the ischaemic border zone. Further, effects of tissue plasminogen activator (tPA) as currently best treatment for stroke and the potentially neuroprotective co-administration of hyperbaric oxygen (HBO) were investigated. Rats underwent middle cerebral artery occlusion and were assigned to control, tPA or tPA+HBO. Twenty-four hours, 7, 14 and 28 days were determined as observation time points. The accumulation of macrophage-like cells was semiquantitatively assessed by CD68 staining in the ischaemic area and ischaemic border zone, and linked to the clinical course. CD11b, ionized calcium binding adaptor molecule 1 (Iba), glial fibrillary acidic protein (GFAP) and Neuronal Nuclei (NeuN) were applied to reveal delayed glial and neuronal alterations. In all groups, the accumulation of macrophage-like cells increased distinctly from 24 hours to 7 days post ischaemia. tPA+HBO tended to decrease macrophage-like cell accumulation at day 14 and 28. Overall, a trend towards an association of increased accumulation and pronounced reduction of the neurological deficit was found. Concerning delayed inflammatory reactions, an activation of microglia and astrocytes with co-occurring neuronal loss was observed on day 28. Thereby, astrogliosis was found circularly in contrast to microglial activation directly in the ischaemic area. This study supports previous data on long-lasting inflammatory processes following experimental stroke, and additionally provides region-specific details on glial reactions. The tendency towards a decreasing macrophage-like cell accumulation after tPA+HBO needs to be discussed critically since neuroprotective properties were recently ascribed to long-term inflammatory processes.
KW  - blood-brain-barrier
KW  - focal cerebral-ischemia
KW  - experimental stroke
KW  - macrophages
KW  - HBO
KW  - tPA
KW  - tumor-necrosis-factor
KW  - inflammatory mechanisms
KW  - mononuclear phagocytes
KW  - astroglia
KW  - microglia
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-133136
VL  - 56
IS  - 2
SP  - 78
EP  - 89
ER  -