TY  - JOUR
TI  - Mouse Transient Global Ischemia Two-Vessel Occlusion Model
AU  - Pontarelli, Fabrizio  
AU  - Ofengeim, Dimitry  
AU  - Zukin, R. Suzanne
AU  - Jonas, Elizabeth A.
VL  - 2
IS  - 18
PY  - 2012
DA  - 2012/09/20
SP  - e262
C1  - Bio-protocol 2012;2:e262
DO  - 10.21769/BioProtoc.262
UR  - https://doi.org/10.21769/BioProtoc.262
AB  - Transient global ischemia in rodents induces delayed death of hippocampal CA1 neurons, as well as in some hilar neurons of the dentate gyrus, medium aspiny neurons of the striatum, pyramidal neurons in neocortical layers II, V and VI, and Purkinje neurons of the cerebellum. In contrast to focal ischemia that mimics regional stroke in humans, this model of global ischemia mimics the brain injury that occurs after human cardiac arrest. Early events include caspase activation, cleavage of anti-death Bcl-2 family proteins and large mitochondrial channel activity. Genetically engineered mice provide opportunities for study such as the knock-in mouse expressing a caspase-resistant form of Bcl-xL found to exhibit markedly reduced mitochondrial channel activity and reduced vulnerability to ischemia-induced neuronal death1. It is therefore relevant to adapt and develop a simple protocol for producing transient global ischemia in mouse2. The two-vessel occlusion model has been specifically developed to provide optimal outcomes in mouse and offers several advantages over the four-vessel occlusion model traditionally used in rat including the relative ease of the procedure as well as only a single day of surgery. However it should be noted that this procedure has a higher morbidity rate compared to other ischemia models as well as a higher degree of variability. These two disadvantages necessitate the use of a larger cohort of animals, which for many healthy breeding transgenic animals is a non-deterring factor.
KW  - Bcl-xL Bcl-2
KW  - Stroke
KW  - Cell death
KW  - Apoptosis
KW  - Mitochondria
JF  - Bio-protocol
SN  - 2331-8325
PB  - Bio-protocol LLC.
BIO101  - False