Oxidative Stress-Induced Damage to the Developing Hippocampus Is Mediated by GSK3β.

Neonatal brain injury renders the developing brain vulnerable to oxidative stress, leading to cognitive deficit. However, oxidative stress-induced damage to hippocampal circuits and the mechanisms underlying long-term changes in memory and learning are poorly understood. We used high oxygen tension or hyperoxia (HO) in neonatal mice of both sexes to investigate the role of oxidative stress in hippocampal damage.

Neonatal brain injury causes cerebellar learning deficits and Purkinje cell dysfunction.

Premature infants are more likely to develop locomotor disorders than term infants. In a chronic sub-lethal hypoxia (Hx) mouse model of neonatal brain injury, we recently demonstrated the presence of cellular and physiological changes in the cerebellar white matter. We also observed Hx-induced delay in Purkinje cell (PC) arborization.

Migratory behavior of cells generated in ganglionic eminence cultures.

Migration of cells is a common process that leads to the development and maturation of the vertebrate central nervous system (Hatten, '99). The cerebral cortex consists of two basic neuronal types: excitatory and inhibitory. These cells arise in distinct areas and migrate into the cortex along different routes (Pearlman et al.

Studies on the use of Cassia singueana in malaria ethnopharmacy.

Cassia singueana (Family: Fabaceae) is used in northern Nigeria for the treatment of acute malaria attack. We investigated the activities of the methanol extract of the root bark of this plant against rodent plasmodia infection, nociception, pyrexia and inflammation in mice and rats. The studies were carried out using acetic acid-induced writhing, hot plate algesia, rodent plasmodia (Plasmodium berghei) in mice; formalin test, yeast-induced pyrexia and egg-albumin-induced inflammation in rats.