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G M Bishop

Publications and source records attributed to G M Bishop.

4 recordsLinked to original sources
PubMed2003

Altered cellular distribution of iron in rat cerebral cortex during the oestrous cycle.

Iron levels in blood, liver and the substantia nigra fluctuate during the oestrous cycle but it is not known whether the cellular distribution also changes. This study shows that during dioestrus, when serum levels of oestradiol are low, the amount of histochemically detectable iron in the cerebral cortex is significantly lower than in proestrus when oestradiol levels are highest. During dioestrus iron is concentrated within neurones, and the transition to proestrus is associated with a shift in iron localisation from neurones to vascular endothelial cells and oligodendrocytes. These data raise the possibility that changes in the concentration of serum oestrogen (or other reproductive hormones) during the oestrous cycle can influence the intercellular transport of iron in the brain.

Animals↗
PubMed2003

Deposits of fibrillar A beta do not cause neuronal loss or ferritin expression in adult rat brain.

In Alzheimer's disease (AD), senile plaques containing amyloid-beta (Abeta) are associated with neurodegeneration, yet little quantitative data are available concerning the spatiotemporal patterns of neuronal death that result from exposure to Abeta deposits. Furthermore, plaques are accompanied by ferritin-rich cells but no data exist regarding the spatiotemporal expression of ferritin in response to Abeta. The present study has obtained such data after injecting aged Abeta peptide into the parietal cortex of adult rats. Injected deposits of fibrillar Abeta (1 microliter of 1 mM in saline) were cleared within 7 days but did not cause a significant increase in ferritin expression. Counts of dying neurones showed that human Abeta1-40 killed as many neurones as control injections of saline, while human Abeta1-42 and rat Abeta1-40 killed significantly less. We conclude that the fibrillar Abeta in plaques is not likely to be directly responsible for the neurodegeneration and ferritin expression that occurs in AD.

Amyloid beta-Peptides↗
PubMed2001

Quantitative analysis of cell death and ferritin expression in response to cortical iron: implications for hypoxia-ischemia and stroke.

Iron that is not bound to storage proteins can catalyse the generation of toxic hydroxyl radicals. Iron can be released from brain storage proteins by hypoxic conditions, such as those that accompany stroke, and the situation can be compounded by iron released from hemoglobin in extravasated blood cells. Despite the neurotoxicity of iron, there is little quantitative data concerning the spatio-temporal extent of its toxicity in vivo. The present study measures the effects of a pathologically relevant concentration of iron (1.0 mM) on neuronal death and on ferritin expression in vivo. Injection of iron (1 microl ferric ammonium citrate) into rat parietal cortex resulted in 7.9-fold more ferritin-labeled cells than did control injections of ammonium citrate at 1 day post-injection. This elevated expression continued for at least 1 week. One day after injection, the mean number of Fluoro-Jade-labeled degenerating neurons in 100 microm sections passing through the center of ferric ammonium citrate injection sites was 664+/-64. This value was 4.5-fold higher than at ammonium citrate injection sites, and this difference increased to 56-fold by day three. By 5 days post-injection, few dying neurons were observed at the control sites, but neurodegeneration continued beyond a week at the iron-injected sites. Thus, iron released during a brief episode of hypoxia-ischemia or during a stroke may be neurotoxic for a protracted period. Therefore, our findings indicate that it may be beneficial to target iron-induced peroxidation throughout the first few weeks following an intracerebral hemorrhage or an hypoxic-ischemic episode.

Animals↗