Why was cognitive im pairment only seen in the diabetic rats afte

Why was cognitive im pairment only seen in the diabetic rats after R M hypoglycemia The present study does not selleck chem provide a clear answer for this, however, we can speculate that less severe oxidative injury in the non diabetic rats or impaired Inhibitors,Modulators,Libraries recovery in the diabetic rats influenced this. In support of these possibilities, we found that R M hypoglycemia reduced MAP2 Inhibitors,Modulators,Libraries intensity Inhibitors,Modulators,Libraries and thickness in the stratum radiatum area of hippocampal CA1, more so in diabetic than in non diabetic rats. Synaptic density in the hippocampus plays a crucial role in memory. For example, synaptic density in the CA1 stratum radia tum is regulated by estrogen, leading to modulation Inhibitors,Modulators,Libraries of long term depression and long term potentiation.

Evidence suggests that diabetes, stress, and aging negatively affect synaptic plasticity in brain regions including the hippocampus and the Inhibitors,Modulators,Libraries cortex, which can lead to persistent inhibition of LTP and facilitation of LTD and in turn might lead to activity dependent synapse weakening and contribute to cognitive impairments. We found that R M hypoglycemia induced oxidative damage in hippocampal dendrites and microglial activa tion was reduced by the NADPH oxidase inhibitor, apocy nin, suggesting a mechanism by which R M hypoglycemia may promote oxidative stress in the hippocampus during reperfusion. Glucose reperfusion induced dendritic in jury results in part from the activation by superoxide produced through NADPH oxidase. NADPH oxidase generates superoxide through a process that requires glu cose as a substrate for NADPH production, such that glucose availability can be the rate limiting factor in superoxide production by this process.

Extrapolating these results LY3009104 to clinical settings has some limitations. The experimental paradigm of hypoglycemia for 5 consecutive days is intended to model recurrent hypoglycemia, but the effects over time of widely spaced hypoglycemic intervals may differ from the tightly spaced recurrences used here. Similarly, the diabetic rats were subjected to much greater variations in glucose than would typically occur in clinical settings. They also were subjected to much greater changes in plasma glu cose than the non diabetic rats, a factor which may have contributed to the differences observed between the dia betic and non diabetic rats. Last, rodent brains may dif fer from human brains in their responses to R M hypoglycemia. Further research, particularly from the translational and clinical perspective is needed to resolve these questions. Background Epileptic seizure is a major form of acute brain damage that could lead to a large number of changes at the cellular level, including oxidative stress, cytokine activation, changes in plasticity or activation of some late cell death pathways.

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