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Early postnatal ethanol exposure induces fluctuation in the expression of BDNF mRNA in the developing rat hippocampus

100%
Miki T., Kuma H., Yokoyama T., Sumitani K., Matsumoto Y., Kusaka T., Warita K., Wang Y.-Y., Hosomi N., Imagawa T., Bedi K. S., Itoh S., Nakamura Y., Takeuchi Y.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 4
484-493
EN
Effects of early postnatal ethanol exposure on brain-derived neurotrophic factor (BDNF) mRNA expression in the rat hippocampus were investigated. Wistar rats were assigned to either ethanol treatment (ET), separation control (SC) or mother-reared control (MRC) groups. Ethanol exposure was achieved by a vapor inhalation method for 3 hours a day between postnatal days (PND) 10-15. On PND 16, 20, 30, and 60, the expression of BDNF mRNA in the hippocampus was determined using real-time RT-PCR analysis. There was a significant age-related increase in the BDNF mRNA expression between PND 3060 in MRC animals. The BDNF mRNA expression in ET rats was increased at both PND 16 and 20 and thereafter decreased at PND 60 compared to SC animals. Such age-related fluctuation in the expression of BDNF mRNA differed from that of MRC animals. The exact functional implications, if any, of these ethanol-induced changes in BDNF mRNA expression remain unknown although it can be speculated that they may have an effect on the behaviors known to be influenced by the hippocampal formation.
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Mismatch negativity in methamphetamine dependence: A pilot study

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Hosak L., Kremlacek J., Kuba M., Libiger J., Cizek J.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 1
97-102
EN
The objective of this study was to verify hypothesised changes in event related potentials (visual mismatch negativity, vMMN) in 17 subjects dependent on methamphetamine (MAMP) compared to age and gender matched 17 healthy volunteers. We found a significant correlation between vMMN and duration of methamphetamine abuse (Spearman correlation coefficient r=0.54 - 0.78; P<0.05). The positive correlation indicates drop of originally more negative response to deviant stimulus, what may indicate a pre-attentive processing enhancement in the first years of MAMP abuse with its decease later on. Accordingly, post-hoc analysis revealed significantly stronger vMMN in patients with length of MAMP abuse shorter than 5 years than in paired controls. There were no such differences in abusers with the length of abuse longer than 5 years. The results show that the visual processing on the pre-attentional level can be influenced by long-term MAMP abuse, what can be specifically assessed by vMMN.
3

Experimental and clinical aspects of neurotoxic effect of aluminium

88%
Nowak P., Brus R.
Postępy Higieny i Medycyny Doświadczalnej
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1996
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vol. 50
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issue 6
621-633
EN
In the paper there were described some problems concerning influence of aluminium on central nervous system mainly. It was shown some aspects of neurotoxic action of aluminium in experimental studies and in some clinical disorders probability connected with intoxication of aluminium.
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Inhibition of neuronal nitric oxide synthase prevents iron-induced cerebellar Purkinje cell loss in the rat

88%
Gulturk S., Kozan R., Bostanci M. O., Sefil F., Bagirici F.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 1
26-31
EN
Iron plays an important role in maintaining normal brain function. However, in many neurodegenerative diseases abnormal iron accumulation in specific brain regions has been consistently reported. In this study, we investigated the neurotoxic effect of the intracerebroventricularly injected iron on the cerebellar Purkinje cells in the rat and the role of nitric oxide (NO) in this process. The role of NO in rats administered iron (FeCl36H2O) was examined with the use of a donor of NO, L-arginine (L-Arg), and a central selective inhibitor of NO synthase, 7-nitroindazole (7-NI). For this reason, rats were divided into 5 groups: control, iron-injected, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI. Means (value ? standard deviation) of the total numbers of Purkinje cells in the cerebellum were estimated as 337 ? 23, 209 ? 16, 167 ? 19, 305 ? 26, and 265 ? 14 thousands in the control, iron, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI groups, respectively. Iron treatment alone and the combination of iron and L-Arg caused a significant reduction in the total number of cerebellar Purkinje cells. Therefore, L-Arg increased the Purkinje cell loss induced by treatment with iron. These data show that inhibition of the neuronal NOS by 7-NI can prevent some of the deleterious effects of iron on cerebellar Purkinje cells. Presence of L-arginine decreased the neuroprotective effect of 7-NI.
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Measurement of nitric oxide in hippocampal slices: induction with nitroso compounds and the effect of depolarization

88%
Haklar G., Saybasili H., Yuksel M., Yalcyn S.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 4
319-325
EN
Nitric oxide not only acts as a messenger for different physiological processes, but also mediates neurotoxicity associated with a variety of neurological disorders including epilepsy. The molecular mechanisms behind these actions are unclear. In this study, we aimed to detect relative amounts of NO released from rat hippocampal slices by chemiluminescence measurements under NMDA stimulation and spontaneous depolarization conditions. Hippocampal slices were preferred because of their functional integrity useful in simulating in vivo conditions. The reliability of the system was verified by administering increasing concentrations of a NO donor sodium nitroprusside in different redox milieu and a NO scavenger, carboxy-2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy PTIO). The redox versatility of NO allows interconversion from neuroprotective to neurotoxic species by a change in the ambient redox milieu. We have quantitated NO formed under NMDA stimulation and spontaneous depolarization conditions, and showed that depolarization increased NO formation and was excitotoxic for the neural tissue.
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Excitotoxic neuronal injury in chronic homocysteine neurotoxicity studied in vitro: The role of NMDA and group I metabotropic glutamate receptors

88%
Zieminska E., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 4
301-309
EN
Elevated homocysteine is a risk factor in cardiovascular diseases and neurodegeneration. Among the putative mechanisms of homocysteine-evoked neurotoxicity, disturbances in methylation processes and NMDA receptor-mediated excitotoxicity have been suggested. Our previous studies demonstrated that group I metabotropic glutamate receptors along with NMDA receptors participate in acute homocysteine-induced neuronal damage. In this study, using propidium iodide staining, we tested whether the same mechanism may mediate chronic homocysteine neurotoxicity. Our results confirmed that the application of D,L-homocysteine in micromolar concentrations for 3 days induces neurodegeneration in primary cultures of cerebellar granule neurons. Uncompetitive NMDA receptor antagonist MK-801, and mGlu1 or mGlu5 receptor antagonists (LY367385 and MPEP, respectively), given alone provided very limited neuroprotection. However, simultaneous application of the NMDA receptor antagonists MK-801, memantine or amantadine and MPEP almost completely prevented chronic homocysteine neurotoxicity. These findings suggest a novel therapeutic strategy to combat neurodegeneration induced by hyperhomocysteinemia comprising a combination of antagonists of group I metabotropic glutamate receptors and NMDA receptors.
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Brain injury: prolonged induction of transcription factors

88%
Pennypacker K. R., Kassed K. C. A., Kassed C. A., Eidizadeh E. S., Eidizadeh S., O. C. J. P., O?Callaghan J. P., O?Callaghan J. P.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 4
515-528
EN
A specific temporal order of events at the cellular and molecular level occurs in response to injury to the brain. Injury-compromised neurons degenerate while surviving neurons undergo neuritogenesis and synaptogenesis to establish neuronal connectivity destroyed in the injury. Several genes, such as those coding cytoskeletal proteins and growth factors, have been shown to be regulated by AP-1 and NF-kB transcription factors, two of the most studied DNA binding regulatory proteins. Our laboratory has discovered that Fos-related antigen-2 from AP-1 transcription factor family and NF-kB p65 and p50 subunits are induced long-term (days to months) in the brain after neurotoxic, excitotoxic or ischemic insult. Fos-related antigen-2 is induced in neurons in several models of injury and its elevated expression lasts days to months, corresponding to the severity. The time-course of FRA-2 induction is abbreviated with less severe insult (terminal damage) relative to the cell death, but the induction occurs during the period of regeneration and repair in both models. NF-kB p65 is basally expressed in hippocampal and cortical neurons, but is elevated in reactive astrocytes in hippocampus and entorhinal cortex starting at two days and lasting at least two weeks after kainate treatment. Neurons of the hippocampus surviving ischemic or neurotoxic injury increase expression of NF-kB p50 for at least a week after injury, suggesting a function for p50 in neuronal survival and/or repair. The extended expression of these transcription factors implies a role in the activation of genes related to repair and regeneration, such as growth factors and synaptic proteins, after injury to the CNS.
8
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Effects of lead on cholinergic SN56 neuroblastoma cells

88%
Jankowska-Kulawy A., Gul-Hinc S., Bielarczyk H., Suszkiw J. B., Pawelczyk T., Dys A., Szutowicz A.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 4
453-462
EN
Age-dependent accumulation of lead in brain has been implicated in the pathomechanisms of Alzheimer.s disease. The aim of this work was to investigate whether cholinotoxic effects of lead may result from alterations in acetyl-CoA metabolism. One day exposure of differentiated SN56 cholinergic neuroblastoma cells to 0.5 mumol/L lead or 0.01 mmol/L amyloid-beta1-42 increased fraction of nonviable cells to about 20%. Suppression of choline acetyltransferase activity occurred only in the presence of fresh amyloid-beta1-42, whereas lead was ineffective. All agents in combination caused suppression of acetyl-CoA in cytoplasm and mitochondria down to 19% and 34% of controls, respectively. Inverse correlation was observed between whole cell acetyl-CoA level and fraction of nonviable cells at different combinations of lead and other neurotoxic compounds. It indicates that lead had no primary suppressive effect on cholinergic phenotype but, at least in part, exerted cytotoxic influence on cholinergic neurons through the decrease of their acetyl-CoA.
9

The role of nitric oxide in the physiological and pathological functions of the central nervous system

88%
Tutka P., Kleinrok Z.
Postępy Higieny i Medycyny Doświadczalnej
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1995
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vol. 49
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issue 2
189-199
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How does trimethyltin affect the brain:facts and hypotheses

88%
Koczyk D.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 2
587-596
EN
Trimethyltin, an organic compound of tin, is a potent neurotoxicant of mechanism of action yet to be uncovered.The neuropathological findings that causes selective hippocampal damage with several unique features, highly reminiscent of Ammon's horn sclerosis as a final result, have rised the possibility that there is a link between trimethyltin neurotoxicity and other degenerative events for which an imbalance between neuronal inhibition/excitation has been proposed.However, there still exist a whole catalog of issues which await clarification.One of the greatest importance is how does trimethyltin reach the critical sites within the brain and what are they ? Available data concerning the long-term consequences related to trimethyltin neurotoxicity are also far from being completed.This review current data from in vitro and in vivo studies on neurotoxic effects of trimethyltin.Several hypotheses on mechanisms that may led to neuronal death induced by the toxin are presented.
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The influence of repeated systemic penicillin injections at subconvulsive doses on spontaneous Spike-Wave Discharges in the rat

88%
Stankiewicz J., Gralewicz S.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 3
673-681
EN
Changes in nonconvulsive spontaneous epileptic activity- Spike-Wave Discharges (SWD) - induced by repeated intraperitoneal (i.P.) administration of crystaline panicillin (CP) at subconvulsive doses were evaluated in imp-DAK rats.Three groups received tan daily i.p.injections of PC at doses of 750.000, 500.000 and 250.000 IU/kg b.w..For comparison, another classic convulsant, penetylenetrazol (PTZ) was applied in the same way to another group.PTZ was also given in CNS excitability.Repeated PC injections resulted in a progressive increase in the basal level of the spontaneous SWD activity and in increase in the SWD response to PC, which was statistically significant in the case of the dose 750.000 IU/kg b.w..Moreover, in all rats given PC the response to PTZ (increase in SWD activity) was reduced.The results obtained in this and previous experiment suggest that in the rat CNS develop which prevent to convulsive effect of Pc but promote the occurence of the spontaneous nonconvulsive SWD activity.
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Neuroprotective effect of ACTH (4-9) in degeneration of hippocampal nerve cells caused by dexamethasone: morphological, immunocytochemical and ultrastructural studies

75%
Sekita-Krzak J., Zebrowska-Lupina I., Czerny K., Stepniewska M., Wrobel A.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 1
1-8
EN
. Sustained exposure to glucocorticosteroids (GCs), adrenal hormones secreted during stress, can cause neural degeneration. This is particularly so in the hippocampus, a principal neural target site for GCs. The purpose of this research was an assessment of the neuroprotective effect of ACTH (4-9) in degenerative changes of hippocampal neurons induced by synthetic GC - dexamethasone. Experiments were conducted on male Albino-Swiss mice. We studied the morphology of neurons in the dorsal hippocampus in slides stained with cresyl violet. Immunocytochemical analysis was carried out with the use of monoclonal antibody anti-MAP2 in order to detect alterations in the the neuronal cytoskeleton. We also performed ultrastructural examinations of hippocampal neurons. Quantitative analysis of morphological changes was completed using a computer analyser of histological pictures. It was shown that dexamethasone administered in toxic doses evokes neuronal death in layer CA3 of the hippocampus. Results indicate that ACTH (4-9) shows protective effects in that model. Dexamethasone-induced damage to hippocampal pyramidal neurons (assessed by cell counts, immunocytochemical analysis of cytoskeletal alterations and ultrastructural studies) was significantly reduced in animals administered ACTH (4-9).
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