Biomedical subjects

D Maresová

Publications and source records attributed to D Maresová.

At least 19 recordsLinked to original sources

PubMed2006

Alcohol abuse in mothers during gravidity and breastfeeding brings changes of hippocampal neurons in their offspring.

Neurotoxic effect of ethanol on the CNS of laboratory rats in the prenatal and postnatal period was studied. Another aim of the experiment was to analyse structure of the hippocampus after the prenatal and postnatal exposure to alcohol and to identify the most vulnerable hippocampal regions. Pregnant Wistar rats of our own breed received 20% alcohol p.o. ad libitum every day since the conception to the 18th day of postnatal life of their offspring. Since the birth (the day 1) till the age of 18 days offspring were kept together with their mother and were exposed to postnatal alcohol effect (alcohol in the breast milk). At the age of 18 days animals were perfused under deep thiopental anaesthesia with buffered solution of paraformaldehyde. Serial sections were stained with Fluoro-Jade B and DNA specific dye bis-benzimide (Hoechst No 33258). Brains of young rats aged 18 days were analysed under the light microscope Olympus Provis AX-70 with epifluorescence. In CA1 and CA3 areas and in Gyrus dentatus of the hippocampus, groups of degenerating cells were observed. In all offspring some cells with fine granulated karyons were identified, which were accompanied with high numbers of glial cells. Our results demonstrate the neurotoxic effects of alcohol and the high vulnerability of the developing CNS. The identification of cells with segmented karyons indicates the role of apoptotic mechanism in the cell death.

Animals↗

PubMed2006

Effect of magnesium pre-treatment on the hippocampal NOS activity during long-lasting intermittent hypoxia.

Influence of magnesium pre-treatment during repetitive hypoxia was studied in the hippocampus of rats by histochemical analysis (NADPH-diaphorase staining). NADPH-diaphorase occurs concurrently with NO-synthase that is responsible for NO synthesis. Rat pups were kept together with their mother for 8 hours a day in a hypobaric chamber at a simulated altitude of 7,000 m since the day of birth till the 17th day. The first group of animals was exposed to the repeated hypoxia; the second group under the same conditions was pre-treated by magnesium before the exposition to the hypoxia. Both groups were compared with intact control animals and intact animals treated with magnesium. The experimental and control animals were the transaortically perfused with 4% buffered neutral formaldehyde under thiopental anaesthesia at the age of 35 days. Brains were processed for NADPH-d staining. We estimated the density of NADPH-d positive neurons in CA1 and CA3 areas of the hippocampus and in the dentate gyrus. Intermittent hypoxia brings about higher numbers of NADPH-diaphorase positive neurons of CA1 and CA3 of the hippocampus and of the dorsal blade of dentate gyrus, in the comparison with either group of control animals. In the hilus and ventral blade of the dentate gyrus, on the contrary, the number of NADPH-d positive neurons was smaller. Magnesium pre-treatment during hypoxia decreased number of nitrergic neurons in all areas of the hippocampus except CA1 area, where the effect of magnesium was not significant. These results demonstrate that magnesium can probably have a neuroprotective effect.

Animals↗

PubMed2005

Influence of magnesium sulphate on evoked activity of rat brain after exposure to short-term hypoxia.

Young Wistar rats (aged 12, 25 and 35 days) were exposed to short-term (60 min) hypobaric hypoxia of 41 kPa. Cortical afterdischarges (ADs) were evoked by repeated direct stimulation of the sensorimotor cortex and the duration of ADs was monitored to examine the influence of magnesium sulphate injection (0.3 g/kg b.w.). In 12-day-old hypoxia-exposed rats, an increase of the mean duration of ADs after the repeated stimulation appeared. This effect was prevented by magnesium administration. In 25- and 35-day-old rats exposed to hypoxia a shortening of ADs was registered but no specific effect of magnesium sulphate pretreatment was observed. The brain susceptibility and ability to terminate evoked seizures is discussed.

Animals↗

PubMed2005

Functional and morphological changes of the brain in rats exposed to intermittent hypobaric hypoxia after the repetitive magnesium administration.

Intermittent hypobaric hypoxia induces functional and morphological changes of the brain in 25-day-old rats. Administration of magnesium has partial pro-convulsion effect in hypoxia not exposed rats and it practically does not influence the excitability of cortical neurones in rats exposed to intermittent hypoxia. Magnesium administration decreases the number of NADPH-diaphorase neurones in rats exposed to hypoxia in all studied areas of the hippocampus and dentate gyrus. In control rats this effect was only in CA1, CA3 and in the ventral blade of the dentate gyrus. Increased concentration of magnesium in cells of the hypoxia exposed rats after the repeated magnesium administration was found.

Animals↗

PubMed2005

Effect of the perinatal alcohol abuse on the development of neuronal population in the hippocampus.

The study deals with neurotoxic effects of alcohol on the CNS of laboratory rats in the prenatal period. The aim of the experiment is to analyse structure of the hippocampus after the prenatal exposure to alcohol and to identify the most vulnerable hippocampal regions. Pregnant Wistar rats of our own breed received alcohol (2 g per 100 g of body i.p.) each day since the first to the last day of pregnancy. Since the birth till the age of 34 days offsprings were kept together with their mother and were not exposed to alcohol. At the age of 35 days animals were perfused under the deep thiopental anaesthesia with buffered solution of paraformaldehyde. In the CA1 area of the hippocampus groups of degenerating cells were observed. In the CA3 area degenerating cells were also found. Some cells with fine granulated karyons were identified, which were accompanied with high number of glial cells. Our results demonstrate the neurotoxic effects of alcohol and the high vulnerability of the developing CNS. Remarkable is the observation of the high number of dying cells 35 days after the last exposition to alcohol. It suggests a long-term process of neuronal circuit remodelling in the juvenile tissue, probably triggered by apoptosis. The identification of cells with fine granulated karyons indicates the role of apoptotic mechanism in the cell death.

Animals↗

PubMed2005

Repeated kainic acid administration and hippocampal neuronal degeneration.

Many animal models have been established to study the mechanisms leading to excitotoxicity. One of the more commonly used models is kainic acid (KA) induced excitotoxicity. Upon administration of KA in rodents, KA produces acute status epilepticus and neuronal damage. The aim of the study was to examine the morphologic alteration in the hippocampus of mature rats, after repeated KA administration. The first group was given KA repeatedly in six doses (10 mg/1000 g), each second day. The second group was given KA i.p. repeatedly in six smaller doses (5 mg/1000 g), each second day. The third group (control animals) received corresponding volumes of the normal saline (5 or 10 mg/1000 g respectively). Animals were transcardially perfused; serial sections were stained with Fluoro-Jade B and DNA-specific dye bis-benzimide (Hoechst). In CA1 region of the first group many degenerating cells were observed. The CA2 region was not as much affected as CA1. In the CA3 region no degenerating cells were observed. In the second group the most prominent was the cell loss both in the CA3 region and in the hilus of the dentate gyrus.

Animals↗

PubMed2005

[Neuronal network].

Function of the central nervous system is based on mutual relations among the nerve cells. Description of nerve cells and their processes, including their contacts was enabled by improvement of optical features of the microscope and by the development of impregnation techniques. It is associated with the name of Antoni van Leeuwenhoek (1632-1723), J. Ev. Purkyne (1787-1869), Camillo Golgi (1843-1926), and Ramón y Cajal (1852-1934). Principal units of the neuronal network are the synapses. The term synapse was introduced into neurophysiology by Charles Scott Sherrington (1857-1952). Majority of the interactions between nerve cells is mediated by neurotransmitters acting at the receptors of the postsynaptic membrane or at the autoreceptors of the presynaptic part of the synapse. Attachment of the vesicles to the presynaptic membrane and the release of the neurotransmitter into the synaptic cleft depend on the intracellular calcium concentration and on the presence of several proteins in the presynaptic element.

Humans↗

PubMed2005

Intermittent hypobaric hypoxia during development--morphological and functional changes in the neocortex.

Infant rats, together with their mother, were exposed to the simulated altitude of 7,000 m for 8 hours per day since birth to the age of 17 days. Animals were studied the 25th day, 8 days after the last exposure to hypoxia. The experimental and control animals were sacrificed the 25th day by the transaortic perfusion with 4% buffered neutral formaldehyde under ether anaesthesia. Brains were processed for classical neurohistological analysis (Nissl staining), Fluoro-Jade B and Hoechst. Cortical area in the AP plane 3 mm posterior to bregma was subjected to quantification and "laminar analysis" of the neurones count. The findings were as follows: a) The cytoarchitectonics of the brain in animals exposed to hypoxia was not severely damaged. b) The thickness of neocortex is in the experimental animals lower than that in the controls. c) The "laminar analysis" of neocortex showed a relative increase of neuronal density in layers I., II., V. and VI. of the cortex. d) The electrical stimulation of sensorimotor cortex 8 days after the end of hypoxia brought about prolongation of evoked cortical after discharges. These results demonstrate that the intermittent hypobaric hypoxia has a profound effect on morphological maturation of the central nervous system in infant rats. Hypoxia influenced the excitation-- inhibition mechanisms of cortical neurones.

Animals↗

PubMed2004

Plasticity of the brain in neuroontogenesis.

Plasticity is a specific endowment of the nervous system to develop, to react or to adjust to the internal and external 'environmental changes, both in the physiological and pathological conditions. Cumulative evidence has revealed the dynamism of the nervous system, based on the balance between the rigidity and plasticity. Different aspects of neuroplasticity can employ common general cellular mechanism. Effects of plasticity can be either positive or negative changes during the development (evolutional plasticity), after the short-term exposition (reactive plasticity), after the long-term or permanent stimuli (adaptational plasticity), and during functional or structural recovery of the damaged neuronal circuits (reparation plasticity). Manifestations of plasticity have probably the same basis, irrespective of a cause, which triggered them, or the brain region where they were accomplished. Activity of neuroplastic processes appears to be especially high in the immature nervous tissue.

Animals↗

PubMed2004

Effect of selenium pre-treatment on evoked cortical afterdischarges in young rats.

Prenatal or perinatal hypoxia is among the most frequent pathogenic factors of encephalopaties. It can induce wide-range of morphological, biochemical, energetic and functional alterations. Accordingly we tested changes of excitability of the sensorimotor cortex in 12, 25 and 35-day-old rats exposed and not exposed to short-term (1 hour) hypobaric and normobaric hypoxia. We studied whether sodium selenate (0,26 mg/kg b.w.) can influence character and/or intensity of evoked cortical afterdischarges or if a pre-treatment by selenium changes effects of hypoxia on such seizures. According to the results we can conclude that in our experiment arrangement sodium selenate only partially alters duration of evoked cortical afterdischarges.

Animals↗

PubMed2004

Changes of evoked epileptic seizures after the short term hypobaric hypoxia in the young rats.

Exposition to the acute intensive hypobaric hypoxia blocks the triggering mechanism of epileptic seizures only within a short time interval after the end of hypoxia period and it does not influence the progressive epileptogenesis in 12-day-old rats. In 25-day-old rats' hypobaric hypoxia suppresses the postictal depression elicited by the repeated stimulation in short interstimulus intervals and it increases the duration of epileptic seizures evoked by electrical stimulation of the sensorimotor cortex.

Age Factors↗

PubMed2001

Excitability changes of cortical neurons during the postnatal period in rats exposed to prenatal hypobaric hypoxia.

Pregnant rats were exposed to intermittent hypobaric hypoxia (at a simulated altitude of 7000 m or 5000 m) and the excitability of cortical neurons of their pups was tested. Stimulation of the sensorimotor cortex of rats prenatally exposed to hypoxia shortened the duration of cortical afterdischarges in 12-day-old rats, but did not change the excitability in 25-day-old animals. Shortening of the first afterdischarge in 35-day-old rats but the prolongation of the first afterdischarge in adult rats (as compared to the duration of cortical afterdischarges in rats not exposed to prenatal hypoxia) were registered. The possible mechanisms of different excitability of cortical neurons in rats prenatally exposed to hypobaric hypoxia are discussed.

Altitude↗

PubMed2001

Carnitine pretreatment can partially change the excitability of the immature nervous tissue.

The possible protective action of L-carnitine on neuronal excitability was studied in 21-day-old male Wistar rats with implanted electrodes. Administration of L-carnitine did not change the elicitation and duration of the epileptic seizures (cortical afterdischarges, ADs) in rats under normobaric oxygen atmosphere conditions. However, in animals exposed to 30 min hypobaric hypoxia the duration of the ADs was shortened after the second, fourth and sixth stimulation (in comparison with the first evoked ADs) while carnitine-treated rats retained their neuronal excitability and the duration of ADs was shortened only after the third stimulation.

Animals↗

PubMed2001

Perinatal complication: hypoxic-ischemic encephalopathy.

The favourable development of foetus is connected with the sufficient oxygen requirement. The brain of the foetus is extraordinarily sensitive to the disorders of oxygen supply. Ischemic brain injury connected with perinatal asfyxia is a frequent cause of hypoxic encephalopathy. An increased tolerance of the brain could be achieved by using peptide grows factors, inhibition of nitric oxide or modifying the glutamate receptors activity. Cerebral hypoxia evolves mainly in the case interruption of the feto-placental circulation or cardiorespiratory failure in the neonate. For making the diagnosis of neonatal encephalopathy is important to determine clinical neurological and systemic deragements in the first few days of life. Assessment of prognosis is generally based on a combination of clinical features and abnormalities of examination methods (electroencephalography, computer tomography).

Asphyxia Neonatorum↗

PubMed2000

Dehydrogenase activity in the blood and brain after adaptation to intermittent hypoxia.

Activities of LDH (lactate dehydrogenase) and alpha-HBDH (alpha-hydroxybutyric dehydrogenase) were measured in rats after intermittent exposure to the aerogenic hypoxia at a simulated altitude of 7000 m during the postnatal period (since birth to the 18th day) or in adulthood (older than the 90th day), except days 6, 7, 13, and 14 of the experiment. Enzymatic activity was measured using standard test kit (Biochemical Test Combination, Boehringer). Twenty hours after the last exposure to hypoxia, the activity of both enzymes was elevated in the serum and in the brain of the young rats. In contrast, in adult rats, the exposure to hypoxia did not result in changes of the enzyme activity in the serum or in the brain. Our results indicate that, whereas in adults the biochemical adaptation to repeated aerogenic hypoxia has no effects on the enzymatic activities of dehydrogenases, the same stimulus during the early postnatal period brings about rising of the aerobic glycolysis contribution to the total energy balance. Such increase is enabled by the increase of LDH and alpha-HBDH activities.

Adaptation, Physiological↗

PubMed1999

Dizocilpine pretreatment suppresses the action of hypoxia on hippocampal epileptic afterdischarges in immature rats.

Effect of dizocilpine (0.5 mg/kg i.p.) on epileptic afterdischarges elicited by low-frequency electrical stimulation of the dorsal hippocampus was studied in rat pups aged 12 and 18 days. Repeated elicitation of afterdischarges (ADs) in control animals resulted in a progressive increase of the duration of ADs in both age groups. Dizocilpine (MK-801) injected after the first afterdischarge suppressed this prolongation in 12-day-old rats only. Hypobaric hypoxia (simulated altitude of 9000 m for one hour) led to a marked prolongation of the first afterdischarge in both age groups with a tendency to shorter ADs after repeated stimulations. Dizocilpine potentiated this tendency in 12-day-old rat pups so that it became statistically significant. Administration of dizocilpine before hypoxia prevented the increase in duration of the first afterdischarge in both age groups.

Animals↗

PubMed1998

[Intermittent hypobaric hypoxia during development--morphologic changes in the neocortex and hippocampus].

Infant rats, together with their mother, were exposed to the simulated altitude of 7,000 m for 8 hours per day since birth to the age of 18 days. Animals were studied the 25th day, 7 days after the last exposure to hypoxia. The experimental and control animals were killed the 25th day by the transaortic perfusion with 4% buffered neutral formaldehyde under ether anaesthesia. Brains were processed for classical neurohistological analysis (Nissl staining). 1. Cortical area in the AP plane 3 mm posterior to bregma were subjected to quantification and "laminar analysis" of the neuron count. 2. Hilus of the dentate gyrus between the AP plane 2.5 mm and 4 mm posterior to bregma were subjected to quantification of the neurons. The findings were as follows: a) The cytoarchitectonics of the brain in animals exposed to hypoxia was not severely damaged. b) The thickness of neocortex is in the experimental animals lower than that in the controls. c) The "laminar analysis" of neocortex showed a relative increase of neuronal density in layers I., II., V. and VI. of the cortex. d) The quantification of the neuron count showed a decrease in hilus of the dentate gyrus. These results demonstrate that the intermittent hypobaric hypoxia has a profound effect on morphological maturation of central nervous system in infant rats.

Altitude↗

PubMed1998

[Postictal depression in 12-day-old animals].

Postictal depression systematically follows epileptic after-discharges (AD) evoked from many different regions of the brain of adult animals. In presented experiments we tested by evoking ADs from sensorimotor cortex whether the susceptibility to undergo postictal depression is age-dependent and whether it correlates with the individual duration of ADs. Groups of 12-, 18- and 25-day-old male rats were used (freely moving animals--semichronic preparations; six trains of rhythmic electrical stimulations in one min. intervals after the end of previous seizure; EEG recordings; durations of ADs were measured). In the whole group of the 25-day-old animals the mean duration of ADs after individual stimulations illustrated the inhibitory influence of the first seizure on the duration of all subsequent ADs. In 18-day-old animals the depression was less pronounced and in 12-day-old it seemed to be not present. Analysis of results in individual animals in the group of youngest animals showed, that duration of pairs of subsequent seizures was related to the duration of the first of them. Also in this age group long seizures caused postictal depression. Duration of seizures seems to vary individually and it strongly influences the mean results of the whole group. The differences between the groups could be explained on the basis of the different pattern of ADs in young and older animals. In young animals the total "output" of seizure is low and it could also cause not so intensive and long posttetanic depression based on changes of intracellular Ca2+, because this form of synaptic plasticity seems to involve the activation of Ca(2+)-dependent protein kinases. Synaptic energy consumption also may play some role in postictal depression occurrence.

Age Factors↗