Abstract
Our previous studies carried out on the pilocarpine model of seizures showed that highly resolved elemental analysis might be very helpful in the investigation of processes involved in the pathogenesis of epilepsy, such as excitotoxicity or mossy fiber sprouting. In this study, the changes in elemental composition that occurred in the hippocampal formation in the electrical kindling model of seizures were examined to determine the mechanisms responsible for the phenomenon of kindling and spontaneous seizure activity that may occur in this animal model. X-ray fluorescence microscopy was applied for topographic and quantitative analysis of selected elements in tissues taken from rats subjected to repetitive transauricular electroshocks (ES) and controls (N). The detailed comparisons were carried out for sectors 1 and 3 of the Ammon’s horn (CA1 and CA3, respectively), the dentate gyrus (DG) and hilus of DG. The obtained results showed only one statistically significant difference between ES and N groups, namely a higher level of Fe was noticed in CA3 region in the kindled animals. However, further analysis of correlations between the elemental levels and quantitative parameters describing electroshock-induced tonic and clonic seizures showed that the areal densities of some elements (Ca, Cu, Zn) strongly depended on the progress of kindling process. The areal density of Cu in CA1 decreased with the cumulative (totaled over 21 stimulation days) intensity and duration of electroshock-induced tonic seizures while Zn level in the hilus of DG was positively correlated with the duration and intensity of both tonic and clonic seizures.
Highlights
Epilepsy, one of the oldest diseases known to mankind and the most common neurological disorder affecting individuals of all ages, is characterized by recurrent spontaneous seizures [1]
Our previous studies carried out on the pilocarpine model of seizures showed that highly resolved elemental analysis might be very helpful in the investigation of processes involved in the pathogenesis of epilepsy, such as excitotoxicity or mossy fiber sprouting
The results presented in this paper confirmed that animal studies aimed at searching for new neuroprotective and antiepileptic drugs should be based on determination of the processes that may be involved in the pathogenesis of neurodegenerative changes and spontaneous seizure activity
Summary
One of the oldest diseases known to mankind and the most common neurological disorder affecting individuals of all ages, is characterized by recurrent spontaneous seizures [1]. The most frequent causes of acquired epilepsies comprise: brain insults including traumatic brain injury, ischemic stroke, intracerebral hemorrhage, infections, tumors, cortical dysplasia, neurodegenerative diseases, and prolonged acute symptomatic seizures [1]. It is long known that there is often a seizure-free period between brain insult and clinical manifestation of seizures [4]. During this silent phase, a cascade of poorly understood processes transforms the non-epileptic brain into the one generating spontaneous recurrent seizures. A better recognition of these pathological processes is necessary to identify potential targets for new antiepileptogenic therapies used after brain insults of different types [5]
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