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Comparison of the influence of two models of mild stress on hippocampal brain - derived neurotrophin factor (BDNF) immunoreactivity in old age rats

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Badowska-Szalewska E. , Ludkiewicz B. , Krawczyk R. , Melka N. , Morys J.

Acta Neurobiologiae Experimentalis

2017

tom 77

nr 1

The way hippocampal neurons function during stress in old age (critical times of life) is dependent on brain derived neurotrophin factor (BDNF). This study examined the influence of acute and chronic forced swim (FS) or high‑light open field (HL‑OF) stimulation on the density of BDNF immunoreactive (ir) neurons in the hippocampal pyramidal layers of CA1, CA2, CA3 regions and the granular layer of dentate gyrus (DG) in old (postnatal day 720; P720) Wistar Han rats. Our data showed that in comparison with non‑stressed rats, acute FS caused a significant increase in the density of BDNF‑ir neurons in CA2 and CA3, while acute HL‑OF led to an increase in this factor in all hippocampal subfields with the exception of DG. However, the density of BDNF‑ir cells remained unchanged after exposure to chronic FS or HL‑OF in the hippocampal regions in relation to the control rats. These results indicate that acute FS or HL‑OF proved to be a stressor that induces an increase in the density of BDNF‑ir pyramidal neurons, which was probably connected with up‑regulation of HPA axis activity and short‑time memory processing of the stressful situation. Moreover, as far as the influence on BDNF‑ir cells in hippocampus is concerned, chronic FS or HL‑OF was not an aggravating factor for rats in the ontogenetic periods studied.

Pyruvate dehydrogenase deficiency: morphological and metabolic effects, creation of animal model to search for curative treatment

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Ebertowska A. , Ludkiewicz B. , Klejbor I. , Melka N. , Morys J.

tom 79

nr 2

The main source of energy for brain and other organs is glucose. To obtain energy for all tissue, glucose has to come through glycolysis; then as pyruvate it is converted to acetyl-CoA by pyruvate dehydrogenase complex (PDC) and finally enters citric acid cycle. What happens when one of these stages become disturb? Mutation in genes encoding subunits of PDC leads to pyruvate dehydrogenase deficiency. Abnormalities in PDC activity result in severe metabolic and brain malformations. For better understanding the development and mechanism of pyruvate dehydrogenase deficiency the murine model of this disease has been created. Studies on a murine model showed similar malformation in brain structures as in the patients suffered from pyruvate dehydrogenase deficiency such as reduced neuronal density, heterotopias of grey matter, reduced size of corpus callosum and pyramids. There is still no effective cure for PDC-deficiency. Promising therapy seemed to be ketogenic diet, which substitutes glucose to ketone bodies as a source of energy. Studies have shown that ketogenic diet decreases lactic acidosis and inhibits brain malformations, but not the mortality in early childhood. The newest reports say that phenylbutyrate increases the level of PDC in the brain, because it reduces the level of inactive form of PDH. Experiments on human fibroblast and zebra fish PDC-deficiency model showed that phenylbutyrate is promising cure to PDC-deficiency. This review summarizes the most important findings on the metabolic and morphological effects of PDC-deficiency and research for treatment therapy. (Folia Morphol 2020; 79, 2: 191–197)

Phenylbutyrate administration reduces changes in the cerebellar Purkinje cells population in PDC‑deficient mice

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Klejbor I. , Mahmood S. , Melka N. , Ebertowska A. , Morys J. , Stachowiak E. K. , Stachowiak M. K. , Patel M. S.

nr 3

In humans, pyruvate dehydrogenase complex (PDC) deficiency impairs brain energy metabolism by reducing the availability of the functional acetyl‑CoA pool. This “hypometabolic defect” results in congenital lactic acidosis and abnormalities of brain morphology and function, ranging from mild ataxia to profound psychomotor retardation. Our previous study showed reduction in total cell number and dendritic arbors in the cerebellar Purkinje cells in systemic PDC‑deficient mice. Phenylbutyrate has been shown to increase PDC activity in cultured fibroblasts from PDC‑deficient patients. Hence, we investigated the effects of postnatal (days 2‑35) phenylbutyrate administration on the cerebellar Purkinje cell population in PDC‑deficient female mice. Histological analyses of different regions of cerebellar cortex from the brain‑specific PDC‑deficient saline‑injected mice revealed statistically significant reduction in the Purkinje cell density and increased cell size of the individual Purkinje cell soma compared to control PDC‑normal, saline‑injected group. Administration of phenylbutyrate to control mice did not cause significant changes in the Purkinje cell density and cell size in the studied regions. In contrast, administration of phenylbutyrate variably lessened the ill effects of PDC deficiency on Purkinje cell populations in different areas of the cerebellum. Our results lend further support for the possible use of phenylbutyrate as a potential treatment for PDC deficiency