The spleen contributes to stroke-induced neurodegeneration.

Stroke, a cerebrovascular injury, is the leading cause of disability and third leading cause of death in the world. Recent reports indicate that inhibiting the inflammatory response to stroke enhances neurosurvival and limits expansion of the infarction. The immune response that is initiated in the spleen has been linked to the systemic inflammatory response to stroke, contributing to neurodegeneration.

Reduced Nuclear Factor kappa B activation in dentate gyrus after active avoidance training.

Nuclear Factor kappa B (NF-kappaB) is a transcription factor associated with neuroplasticity and neuronal survival during injury. Although NF-kappaB has been proven to be involved in various processes of repair, there is also evidence that NF-kappaB is associated with learning and memory formation. Our laboratory has previously observed that mice lacking the NF-kappaB p50 subunit are not proficient in learning tasks associated with active avoidance training, an effective learning paradigm.

Sigma receptor activation reduces infarct size at 24 hours after permanent middle cerebral artery occlusion in rats.

The only available treatment for embolic stroke is recombinant tissue plasminogen activator, which must be administered within three hours of stroke onset. We examined the effects of 1,3-di-o-tolyguanidine (DTG), a high affinity sigma receptor agonist, as a potential treatment for decreasing infarct area at delayed time points. Rats were subjected to permanent embolic middle cerebral artery occlusion (MCAO) and allowed to recover before receiving subcutaneous injections of 15 mg/kg of DTG at 24, 48, and 72 hours.