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In the present work, synchrotron radiation Fourier-transform infrared (SRFTIR) and Raman microspectroscopies were used to evaluate a possible role of creatine in the pathogenesis and progress of pilocarpine-evoked seizures and seizure-induced neurodegenerative changes in the rat hippocampal tissue. The main goal of this study was to identify creatine deposits within the examined brain area, to analyze their frequency in epileptic animals and naive controls and to examine correlations between the number of inclusions in the hippocampal formation of epileptic rats and the quantitative parameters describing animal behavior during 6-h observation period after pilocarpine injection. The presence of creatine in the brain tissue was confirmed based on the vibrational bands specific for this compound in the infrared and Raman spectra. These were the bands occurring at the wavenumbers around 2800, 1621, 1398, and 1304 cm−1 in IR spectra and around 1056, 908 and 834 cm−1 in the Raman spectra. Creatine was detected in eight of ten analyzed epileptic samples and in only one of six controls under the study. The number of deposits in epileptic animals varied from 1 to 100 and a relative majority of inclusions were detected in the area of the Dentate Gyrus and in the multiform hippocampal layer. Moreover, the number of creatine inclusions was positively correlated with the total time of seizure activity.Electronic supplementary materialThe online version of this article (doi:10.1007/s00216-011-5488-z) contains supplementary material, which is available to authorized users.

Epilepsy, the third most common neurological disorder, is characterized by recurrent unprovoked seizures. Although the mechanisms of epileptic convulsions have been a subject of intensive investigations for many years in most cases the etiology of the disease is not known [1].Metallic elements participating in the processes like: oxidative stress, excitotoxicity, mitochondrial dysfunction or protein aggregation may lead to the atrophy and death of neurons in case of some neurodegenerative disorders [2][3][4]. Because epileptic seizures induce neurodegeneration in selected areas of brain it is suspected that metals may be involved in the pathogenesis and progress of epilepsy as well [5].Existing evidence suggests that epileptic seizures significantly change metabolism and distribution of trace elements in the nervous tissue [6][7][8]. From the other hand, content of metals determinates susceptibility to convulsions [9].In our experiment we used pilocarpine in order to induce epilepsy in rats. In order to find what elements are involved in the pathogenesis and progress of epileptic convulsions the comparison between pilocarpine treated and control rats was done. The samples of rat brain were cut using a cryomicrotome into 15 µm thick slices. Thin tissue sections were mounted on Ultralene foil and freeze-dried.X-ray fluorescence microscopy was employed for topographic and quantitative analysis of selected metals in the areas of brain tissue involved in epilepsy. The measurements were done on the bending magnet beamline L at HASYLAB. The multilayer monochromator was applied and the primary photon energy was set to 17 keV. The beam was focused with polycapillary optics for a final beam spot dimension of 15 µm x 15 µm. The characteristic X-ray lines were measured using the Vortex SDD detector from SII Nano Technology USA inc. and the time of spectra acquisition was equal to 6 s per pixel. Measurements of NIST standard reference materials (SRM 1833 and SRM 1832) were performed for spectrometer calibration.The elements such us P, S, Cl, K, Ca, Fe, Cu, Zn, Br, Rb and Sr were detected in rat brain sections. For each sample two-dimensional analysis of elemental distribution was performed for the area of hippocampus and brain cortex. The results of such analysis for selected control and epileptic sample were shown in Figures 1 and 2 respectively.For four regions of hippacampus formation (CA1 -Cornu Ammonis, CA3, DG -Dentate Gyrus and H -Hilus) and motor cortex the mean masses per unit area were evaluated. The areas taken into account in calculations were equal to 300 µm per 300 µm. The preliminary results showed that the level of Ca tends to be higher for CA1 region of hippocampus and cortex in case of animals with pilocarpine induced epilepsy. The opposite relation was observed for Zn level in the area of DG.1551

BackgroundObesity is a worldwide epidemic with more than 600 million affected individuals. Human studies have demonstrated some alterations in brains of otherwise healthy obese individuals and elevated risk of neurodegenerative disease of old age; these studies have also pointed to slightly diminished memory and executive functions among healthy obese individuals. Similar findings were obtained in animal models of obesity induced by high fat diet. On the other hand, low carbohydrate high fat diets are currently promoted for losing weight (e.g., Atkin’s style diets). However, the long-term effects of such diets are not known. Additionally, high fat diets leading to (mild) ketonemia were shown to improve brain function in elderly humans and in some animal models.AimTo evaluate the hypothesis that long-term use of a high fat diet was associated with decreases in spatial memory, smaller hippocampi and hippocampi metabolite concentrations in Wistar rats.MethodsTwenty five male Wistar rats were put on high fat diet (HFD; 60% calories from fat, 30% from carbohydrates) on their 55th day of life, while 25 control male rats (CONs) remained on chow. Adequate levels of essential nutrients were provided. Both groups underwent memory tests in 8-arm radial maze at 3rd, 6th, 9th, and 12th month. 1H magnetic resonance spectroscopy was employed to measure concentrations of tNAA (marker of neuronal integrity) at one month and one year, whereas MRI was used to evaluate hippocampal volumes.ResultsObese rats (OBRs) consumed similar amount of calories as CONs, but less proteins. However, their protein intake was within recommended amounts. Throughout the experiment OBRs had statistically higher concentrations of blood ketone bodies than CONs, but still within normal values. At post-mortem assessment, OBRs had 38% larger fat deposits than CONs (p<0.05), as evaluated by volume of epididymis fat, an acknowledged marker of fat deposits in rats. Contrary to our expectations, OBRs had better scores of memory behavioral tasks than CONs throughout the experiment. At one year, their hippocampi were by 2.6% larger than in CONs (p = 0.05), whereas concentration of tNAA was 9.8% higher (p = 0.014).ConclusionLong-term HFD in our study resulted in better memory, larger hippocampal volumes, as well as higher hippocampal metabolite concentrations, possibly due to increased levels of blood ketone bodies. The results should be interpreted with caution, as results from animal models do not necessarily directly translate in human condition.

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