April 2011

Document Type


Degree Name



Oregon Health & Science University


Cerebellar Purkinje cells (PCs) are vulnerable to ischemic injury and excitotoxicity. The large excitatory input from climbing fibers and parallel fibers are thought to underlie the sensitivity of PCs to ischemia. PCs also have uniquely large numbers of GABAergic contacts with inhibitory interneurons, providing an endogenous method of controlling excitation. However, increasing GABAergic neurotransmission as a neuroprotective strategy has not been thoroughly tested in the cerebellum. The goal of this work was to investigate the neuroprotective mechanisms of the GABA-active neurosteroid allopregnanolone and reveal the effects of ischemia on PC GABA[subscript A] receptor function. Experiments were performed on primary cerebellar neuronal cultures subjected to in vitro ischemia (oxygen-glucose deprivation; OGD), and on an in vivo mouse model of cardiac arrest and cardiopulmonary resuscitation to induce global cerebral ischemia. I initially tested the hypothesis that ischemia causes a rapi




Neuroscience Graduate Program


School of Medicine



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