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Who are responsible for protecting against neuron and synapse injury in immature rats?

July 17th, 2014
Who are responsible for protecting against neuron and synapse injury in immature rats?
Through transmission electron microscopy, it is known that fructose-1,6-diphosphate at 1,000 mg/kg administered intraperitoneally can alleviate rough endoplasmic reticulum degranulation (arrow) in hippocampal CA1 region of rats with repeated febrile convulsions. Credit: Neural Regeneration Research

Fructose-1,6-diphosphate is a metabolic intermediate that promotes cell metabolism. Whether it can alleviate hippocampal neuronal injury caused by febrile convulsion remains unclear.

Dr. Jianping Zhou, the Second Affiliated Hospital, Medical College of Xi'an Jiaotong University, China and his team established a repetitive febrile convulsion model in rats aged 21 days, equivalent to 3–5 years in humans, intraperitoneally administered fructose-1,6-diphosphate at 1,000 mg/kg into the rat model. Results showed that high-dose fructose-1,6-diphosphate reduced mitochondrial swelling, rough endoplasmic reticulum degranulation, Golgi dilation and synaptic cleft size, and increased synaptic active zone length, postsynaptic density thickness, and synaptic interface curvature in the hippocampal CA1 area. The present findings suggest that fructose-1,6-diphosphate is a neuroprotectant against hippocampal neuron and synapse damage induced by repeated febrile convulsion in immature rats.

These results were published in Neural Regeneration Research (Vol. 9, No. 9, 2014).

More information:
Zhou JP, Wang F, Zhang J, Gao H, Yang YF, Fu RG. Repeated febrile convulsions impair hippocampal neurons and cause synaptic damage in immature rats: neuroprotective effect of fructose-1,6-diphosphate. Neural Regen Res. 2014;9(9):937-942.

Provided by Neural Regeneration Research

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