bryostatin-1 and Hypoxia

bryostatin-1 has been researched along with Hypoxia* in 1 studies

Other Studies

1 other study(ies) available for bryostatin-1 and Hypoxia

Article	Year
Poststroke neuronal rescue and synaptogenesis mediated in vivo by protein kinase C in adult brains. Proceedings of the National Academy of Sciences of the United States of America, 2008, Sep-09, Volume: 105, Issue:36 Global cerebral ischemia/hypoxia, as can occur during human stroke, damages brain neural networks and synaptic functions. The recently demonstrated protein kinase C (PKC) activation-induced synaptogenesis in rat hippocampus suggested the potential of PKC-mediated antiapoptosis and synaptogenesis during conditions of neurodegeneration. Consequently, we examined the effects of chronic bryostatin-1, a PKC activator, on the cerebral ischemia/hypoxia-induced impairment of synapses and neurotrophic activity in the hippocampal CA1 area and on hippocampus-dependent spatial learning and memory. Postischemic/hypoxic bryostatin-1 treatment effectively rescued ischemia-induced deficits in synaptogenesis, neurotrophic activity, and spatial learning and memory. These results highlight a neuroprotective signaling pathway, as well as a therapeutic strategy with an extended time window for reducing brain damage due to stroke by activating particular PKC isozymes. Topics: Aging; Animals; Behavior, Animal; Bryostatins; Cell Differentiation; Cell Survival; Enzyme Activation; Hypoxia; Isoenzymes; Learning; Male; Memory; Microscopy, Electron; Neurons; Protein Kinase C; Rats; Rats, Wistar; Stroke; Synapses	2008

Article

Year

Poststroke neuronal rescue and synaptogenesis mediated in vivo by protein kinase C in adult brains.

Proceedings of the National Academy of Sciences of the United States of America, 2008, Sep-09, Volume: 105, Issue:36

Global cerebral ischemia/hypoxia, as can occur during human stroke, damages brain neural networks and synaptic functions. The recently demonstrated protein kinase C (PKC) activation-induced synaptogenesis in rat hippocampus suggested the potential of PKC-mediated antiapoptosis and synaptogenesis during conditions of neurodegeneration. Consequently, we examined the effects of chronic bryostatin-1, a PKC activator, on the cerebral ischemia/hypoxia-induced impairment of synapses and neurotrophic activity in the hippocampal CA1 area and on hippocampus-dependent spatial learning and memory. Postischemic/hypoxic bryostatin-1 treatment effectively rescued ischemia-induced deficits in synaptogenesis, neurotrophic activity, and spatial learning and memory. These results highlight a neuroprotective signaling pathway, as well as a therapeutic strategy with an extended time window for reducing brain damage due to stroke by activating particular PKC isozymes.

Topics: Aging; Animals; Behavior, Animal; Bryostatins; Cell Differentiation; Cell Survival; Enzyme Activation; Hypoxia; Isoenzymes; Learning; Male; Memory; Microscopy, Electron; Neurons; Protein Kinase C; Rats; Rats, Wistar; Stroke; Synapses

2008