71 research outputs found

    Endopiriform nucleus connectivities: the implications for epileptogenesis and epilepsy

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    Several anterograde and retrograde tracing studies have provided detailed information on the afferent and efferent projections as well as the intrinsic connectivities of the endopiriform nucleus (EN). Here, we summarise EN connectional data and the principles of their organisation and discuss the role they may play in the development and spread of epileptic seizures

    Minocycline but not valproic acid influence the density of NogoA-immunoreactive neurons in the hilus of the dentate gyrus of the rats subjected to intracerebral haematoma

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    Intracerebral haemorrhage is a devastating neurological disease with high mortality rate and poor prognosis. The most prominent manifestation of the disease arethe movement disorders, but many patients also suffer from cognitive impairment. Taking into account vulnerability of the neurons located within the hilus of the dentate gyrus (HDG) to many brain insults we decided to study the effectof experimentally induced intracerebral haematoma on density of neurons expressing NogoA protein in HDG. In addition, we studied how administration of valproic acid and minocycline, the two drugs generally believed to be neuroprotective agents, influences the density of these neurons. Our study revealed that 4 weeks after intracerebral haematoma induction, minocycline and valproic acid treatment increased the densities of NogoA-ir neurons in the hilus of contralateral dentate gyrus once the data were compared to ipsilateral hemispheres within the same group. The analysis of contralateral hemisphere data, however, revealed increased densities of NogoA-positive neurons in haematoma and valproic acidtreated animals when compared to contralateral hemispheres of control animals.The administration of minocycline was, however, able to alleviate this increase.These changes may influence the haematoma-induced reorganisation of neuronal circuitries in the dentate gyrus

    Hippocampal-Dependent Spatial Memory in the Water Maze is Preserved in an Experimental Model of Temporal Lobe Epilepsy in Rats

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    Cognitive impairment is a major concern in temporal lobe epilepsy (TLE). While different experimental models have been used to characterize TLE-related cognitive deficits, little is known on whether a particular deficit is more associated with the underlying brain injuries than with the epileptic condition per se. Here, we look at the relationship between the pattern of brain damage and spatial memory deficits in two chronic models of TLE (lithium-pilocarpine, LIP and kainic acid, KA) from two different rat strains (Wistar and Sprague-Dawley) using the Morris water maze and the elevated plus maze in combination with MRI imaging and post-morten neuronal immunostaining. We found fundamental differences between LIP- and KA-treated epileptic rats regarding spatial memory deficits and anxiety. LIP-treated animals from both strains showed significant impairment in the acquisition and retention of spatial memory, and were unable to learn a cued version of the task. In contrast, KA-treated rats were differently affected. Sprague-Dawley KA-treated rats learned less efficiently than Wistar KA-treated animals, which performed similar to control rats in the acquisition and in a probe trial testing for spatial memory. Different anxiety levels and the extension of brain lesions affecting the hippocampus and the amydgala concur with spatial memory deficits observed in epileptic rats. Hence, our results suggest that hippocampal-dependent spatial memory is not necessarily affected in TLE and that comorbidity between spatial deficits and anxiety is more related with the underlying brain lesions than with the epileptic condition per se

    Influence of Short-Term Glucocorticoid Therapy on Regulatory T Cells In Vivo

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    Background: Pre- and early clinical studies on patients with autoimmune diseases suggested that induction of regulatory T(Treg) cells may contribute to the immunosuppressive effects of glucocorticoids(GCs). Objective: We readdressed the influence of GC therapy on Treg cells in immunocompetent human subjects and naı¨ve mice. Methods: Mice were treated with increasing doses of intravenous dexamethasone followed by oral taper, and Treg cells in spleen and blood were analyzed by FACS. Sixteen patients with sudden hearing loss but without an inflammatory disease received high-dose intravenous prednisolone followed by stepwise dose reduction to low oral prednisolone. Peripheral blood Treg cells were analyzed prior and after a 14 day GC therapy based on different markers. Results: Repeated GC administration to mice for three days dose-dependently decreased the absolute numbers of Treg cells in blood (100 mg dexamethasone/kg body weight: 2.861.86104 cells/ml vs. 336116104 in control mice) and spleen (dexamethasone: 2.861.96105/spleen vs. 956226105/spleen in control mice), which slowly recovered after 14 days taper in spleen but not in blood. The relative frequency of FOXP3+ Treg cells amongst the CD4+ T cells also decreased in a dose dependent manner with the effect being more pronounced in blood than in spleen. The suppressive capacity of Treg cells was unaltered by GC treatment in vitro. In immunocompetent humans, GCs induced mild T cell lymphocytosis. However, it did not change the relative frequency of circulating Treg cells in a relevant manner, although there was some variation depending on the definition of the Treg cells (FOXP3+: 4.061.5% vs 3.461.5%*; AITR+: 0.660.4 vs 0.560.3%, CD127low: 4.061.3 vs 5.063.0%* and CTLA4+: 13.8611.5 vs 15.6612.5%; * p,0.05). Conclusion: Short-term GC therapy does not induce the hitherto supposed increase in circulating Treg cell frequency, neither in immunocompetent humans nor in mice. Thus, it is questionable that the clinical efficacy of GCs is achieved by modulating Treg cell numbers

    The projection of the amygdaloid nuclei to various areas of the limbic cortex in the rat

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    The connections of the amygdaloid body with the areas of the limbic cortex in the rat were studied by means of the method on the axonal retrograde transport of the fluorescent tracer Fluoro-Gold. The tracer was injected into the anterior and posterior limbic cortices (cingulate gyrus, granular- and agranular retrosplenial area, respectively. The localization of the corresponding amygdalar- projection zones was investigated and the semiquantitative analysis of the connections was conducted. The projection zones in the rat amygdaloid body are organized topographically. Administration of the fluorescent tracer to the anterior and posterior part of the limbic cortex in the rat (cingulate gyrus and both retrosplenial areas, respectively) reveals labeling of cells only for injections to the former one. The labeled cells were present only in the major components of the basolateral amygdaloid complex. The main source of this projection was anterior part of basolateral nucleus (BLA). Some labeled neurons were found in the lateral nucleus and few in the ventral part of basolateral nucleus. No labeled cells were found within the basomedial nucleus
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