Effect of ketogenic diet on hippocampus synaptic reorganization and GluR5, GluR6 mRNA in kainic acid induced model
- VernacularTitle:生酮饮食对海藻酸致痫大鼠海马突触重建和GluR5、GluR6 Mrna的影响
- Author:
Xu XIANG-PING
1
;
Sun RUO-PENG
;
Jin RUI-FENG
Author Information
1. 山东大学附属齐鲁医院
- Keywords:
ketogenic diet;
epilepsy;
glutamate receptor;
mossy fiber sprouting;
behavior
- From:
Neuroscience Bulletin
2005;21(6):418-424
- CountryChina
- Language:Chinese
-
Abstract:
Objective Ketogenic diet(KD) is a high fat, low protein, low carbohydrate diet. Its antiepileptic effect is certain but the underlying mechanism is unknown. The aim of the study is to reveal the possible antiepileptic mechanism of KD treatment from the view points of synaptic reorganization and GluR5,GluR6 mRNA in hippocampus. Methods Sprague-Dawley rats were induced by kainic acid (KA) at postnatal day 28 as experimental group, control animals were injected the same volume of saline. Animals from each group were divided into two parts, each of which was fed normal rodent chow or ketogenic diet for 8 weeks. Spontaneous recurrent seizures were recorded. Spatial learning and memory ability was evaluated by Morris water maze. Mossy fiber sprouting and neuron damage in hippocampus were investigated by Timm staining and Nissl staining. RT-PCR method was applied to detect the expression of GluR5, GluR6 mRNA in hippocampus. Results KD-fed rats had significantly fewer spontaneous recurrent seizures(1.40±1.03) than control diet-fed rats(7.36±3.75). In water maze testing, all groups demonstrated improvement in water maze performance with significantly decreased escape latencies during the testing days(F=33.93 , P<0.001),but no significant differences were found in the time to platform among the four groups(F=1.24 , P=0.32). The mean A of mossy fiber sprouting in the inner molecular layer of dentate gyrus was markedly higher in KA-induced animals than that in saline control animals but it was similar in different diet-fed groups. No differences were found in the mean A of Timm staining in CA3 area and Nissl staining of neurons in hilus, CA3 and CA1 areas. In KA+KD group rats, GluR6 mRNA was statistically higher (48.16±11.53) than that in KA+ND group rats(30.57±15.57, t=2.40, P<0.05), but no significant difference of GluR5mRNA was found in these two groups (t'=-0.09, P>0.05). Conclusion KD had prominent antiepileptic effect on KA-induced rats and it had no significant impairment on spatial learning and memory for the developing brain. KD can not prevent the MFS in young KA-induced rats, but it may play its antiepileptic role by keeping the high level expression of GluR6 mRNA in the hippocampus, due to its specific neuroprotective action, to inhibit the excitatory transmission at the MF pathway.
