Effects Of CSE To Hippocampus
Previous report have shown that following an SE, reactive astrocytes become hypertrophic (increasing the expression of intermediate filament proteins), and develop longer and thicker processes (Robel et al., 2015),
In this study, astrocytic reaction observed in the GSP or DZP treated CSE is moderate (Plate 4.13.5b), due to the fairly stabled morphology. This could probably be linked to a reduced excitotoxicity or attenuated ROS by GSP or DZP within the hippocampus attributable to GSP treatment especially. It therefore becomes a suggestive evidence from this study that astrocytic reaction in CSE treated with either GSP or DZP is an adaptive type of astriogliosis (a defensive reaction aiming to restore homeostasis).
The functional and morphologic changes astrocytes undergo in the GSP or DZP brain and during CSE may have a dual nature based on the underlying pathophysiological characteristics. On the one hand, reactive astrogliosis can occur as a compensatory mechanism following damage to the nervous system and lead to the reduction in excitability (Vargas-Sánchez et al., 2018). In this study, there was intensification of astrocytic proliferative in the CSE + NS at 7th day post CSE.
This is in consonant with the findings of Gibbons et al. (2013) that in early stages of SE there is no marked intensification in astrocytic proliferation, while at later stages, there is a rapid increase in the number of astrocytes. Although astrocytes have the capacity to proliferate just after an SE, the reported small number of new cells suggest that in models of SE reactive astrocytes are comprised mainly of the resident astrocytes present before the insult (Gibbons et al., 2013).
The major consequential effects of CSE is on higher order behaviour, most especially on indices of learning and memory which is mainly controlled by the hippocampus. These effects of CSE stemmed from reduction in percentage body weight gain, attenuation in the relative hippocampal weight to the brain, decreased spatial and object recognition memory.
However, memory impairment observed in this study was attributed to alteration in the cholinergic neurotransmitters, increased excitotoxicity, pro-oxidant/ antioxidant imbalance which led to exacerbation of oxidative stress of the hippocampus, hippocampal atrophy and necrosis, astriogliosis, and generation of abnormal granule cells in the hillus of the dentate gyrus, All these dysfunction were significantly attenuated by GSP treatment, the effect that was better tolerated than that of a conventional anticonvulsant drug- DZP. It is therefore concluded that GSP can be used is a better agent in the treatment of CSE due to its attenuation in memory impairment and insignificant adverse effects.
The principal goal of CSE treatment is the termination of seizure with little or no attendant on-toward side effects. It is evident from this study that apart from the fact that GSP (20 mg/kg or 10mg/kg) attenuated hippocampal excitotoxicity and astriogliosis following CSE, it also posed no significant side effects on the indices of learning and memory. This study therefore recommends further experimental research on the anticonvulsant and neuroprotective activities of GSP.