Aqueous Extract of Cola nitida and Garcinia kola Synergistically Enhances Hippocampal-hypothalamic Glutamate and Na+ /K+ -ATPase Activity in Male Wistar Rats.

BACKGROUND: The incidence of cognitive decline has been proposed to rise exponentially in the coming years. Therapies targeting molecular pathways involved in the enhancement of memory and energy regulation could be a major breakthrough in the prevention or management of dementia in susceptible populations. OBJECTIVES: This study investigated the effects of aqueous extracts of Cola nitida (AECONS) and Garcinia kola (AEGAK) on glutamate level and Na+/K+-ATPase activity in the hippocampus and hypothalamus of male Wistar rats. METHODS: Adult male Wistar rats (170-200) were randomly allotted into groups (n=5/group); control (distilled water p.o.), AECONS1 (200 mg/kg), AECONS2 (400 mg/kg), AEGAK1 (200 mg/kg), AEGAK2 (400 mg/kg), AECONS1+AEGAK1 and AECONS2+AEGAK2. The extract was prepared and the administration was done daily for 6 weeks. RESULTS AND DISCUSSION: Administration of AECONS or AEGAK increased plasma, hippocampal and hypothalamic glutamate, Na+/K+-ATPase activity, NO, SOD except hippocampal glutamate in AECONS1/AEGAK1, Na+/K+-ATPase activity and SOD in AEGAK1, hypothalamic glutamate and SOD in AECONS1 when compared with control. Besides, MDA level decreased in AEGAK2 and hippocampal but not hypothalamic MDA decreased in AEGAK1 compared with control. However, concomitant administration of AECONS and AEGAK enhanced plasma, hippocampal and hypothalamic biomarkers except hypothalamic MDA level. The present study demonstrates that AECONS and AEGAK synergistically enhance hippocampal and hypothalamic glutamate and Na+/K+- ATPase activity, which are accompanied by NO and SOD-dependent antioxidant enrichment. CONCLUSION: These findings, therefore, suggest that AECONS+AEGAK could be a better therapeutic candidate in hippocampal-hypothalamic-related neurodegenerative diseases.

Upregulation of hippocampal synaptophysin, GFAP and mGluR3 in a pilocarpine rat model of epilepsy with history of prolonged febrile seizure.

Despite the increasing interest and efforts to prevent, treat, and control epilepsy and its clinical manifestation (seizure), the prevalence has not decreased due to incomplete understanding of its etiology. The present study aimed at determining the effect of prolonged febrile seizure (PFS) on the onset of seizure in pilocarpine rat model of temporal lobe epilepsy (TLE). After induction of PFS at postnatal day (PND) 14 in ten out of thirty pups, epilepsy was induced with 350 mg/kg of pilocarpine on PND 60 in the 10 rats with PFS and 10 from the saline group. Animals that met the criteria for TLE were then chosen for the study. Effects of PFS on status epilepticus and the development of spontaneous recurrent seizures (SRSs) were observed. The hippocampal synaptophysin, glial fibrillary acidic protein (GFAP) with metabotropic glutamate receptor 3 (mGluR3) expressions were also measured with LI Cor Tissue florescence, immunofluorescence and immunohistochemistry respectively. We found that PFS reduced the onset of status epilepticus, but had no influence on the development of SRSs. Also, there was no difference in the hippocampal expression of synaptophysin and GFAP between rats that had pilocarpine with or without background PFS. However, the mGluR3 expression was significantly higher in pilocarpine with PFS when compared to pilocarpine alone. Our result showed that PFS may lead to epilepsy. It is also obvious that epilepsy with or without PFS history affects neurochemical expression of synaptophysin, GFAP and mGluR3, hence these proteins may be good targets for drug therapy in reducing both the mortality and morbidity of the disease.