Search results

1

Age-related alteration of poly(ADP-ribose) polymerase activity in different parts of the brain.

100%

Strosznajder J. B., Jęśko H., Strosznajder R. P.

Acta Biochimica Polonica

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2000

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vol. 47

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issue 2

331-337

EN

Poly(ADP-ribose) polymerase (PARP) is a conserved enzyme involved in the regulation of DNA repair and genome stability. The role of PARP during aging is not well known. In this study PARP activity was investigated in nuclear fractions from hippocampus, cerebellum, and cerebral cortex of adult (4 months), old adult (14 months) and aged (24-27 months) rats. Concomitantly, the free radical evoked lipid peroxidation was estimated as thiobarbituric acid reactive substances (TBARS). The specific activity of PARP in adult brain was about 25, 21 and 16 pmol/mg protein per min in hippocampus, cerebellum and cerebral cortex, respectively. The enzyme activity was higher in all investigated parts of the brain of old adults. In aged animals PARP activity was lower in hippocampus by about 50%, and was unchanged in cerebral cortex and in cerebellum comparing to adult rats. The concentration of TBARS was the same in all parts of the brain and remained unchanged during aging. There is no direct correlation between PARP activity and free radical evoked lipid peroxidation during brain aging. The lowered enzyme activity in aged hippocampus may decrease DNA repair capacity which subsequently may be responsible for the higher vulnerability of hippocampal neurons to different toxic insults.

2

Isolation and characterization of novel human short-chain dehydrogenase/reductase SCDR10B which is highly expressed in the brain and acts as hydroxysteroid dehydrogenase*

100%

Huang C., Wan B., Gao B., Hexige S., Yu L.

Acta Biochimica Polonica

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2009

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vol. 56

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issue 2

279-289

EN

Hydroxysteroid dehydrogenase belongs to the subfamily of short-chain dehydrogenases/reductases (SDR), and 11-β-hydroxysteroid dehydrogenase catalyzes the interconversion of inactive glucocorticoids (cortisone in human, dehydrocorticosterone in rodents) and active glucocorticoids (cortisol in human, corticosterone in rodents). We report here the cloning and characterization of a novel human SDR gene SCDR10B which encodes a protein with similarity to 11β-hydroxysteroid dehydrogenase 1. SCDR10B was isolated from a human brain cDNA library, and was mapped to chromosome 19p13.3 by browsing the UCSC genomic database. It contains an ORF with a length of 858 bp, encoding a protein with a transmembrane helix and SDR domain. Its molecular mass and isoelectric point are predicted to be 30.8 kDa and 10.3 kDa, respectively. SCDR10B protein is highly conserved in mammals and fish. Phylogenetic tree analysis indicated that SCDR10B stands for a new subgroup in the 11β-hydroxysteroid dehydrogenase family. Northern blot analysis showed that SCDR10B was highly expressed in brain, and a strong expression signal was detected in hippocampal neurons by immunohistochemical analysis. RT-PCR and immunohistochemical analysis showed that SCDR10B was up-regulated in lung-cancer cell lines and human lung cancer. SCDR10B can catalyze the dehydrogenation of cortisol in the presence of NADP+, and therefore it is a hydroxysteroid dehydrogenase.

3

Plasma membrane Ca2+ -ATPase in excitable and nonexcitable cells.

100%

Żylińska L., Soszyński M.

Acta Biochimica Polonica

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2000

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vol. 47

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issue 3

529-539

EN

There is a significant number of data confirming that the maintenance of calcium homeostasis in a living cell is a complex, multiregulated process. Calcium efflux from excitable cells (i.e., neurons) occurs through two main systems - an electrochemically driven Na+/Ca2+ exchanger with a low Ca2+ affinity (K0.5 = 10-15 μM), and a plasmalemmal, specific Ca2+-ATPase, with a high Ca2+ affinity (K0.5 < 0.5-1 μM), whereas in nonexcitable cells (i.e., erythrocytes) the calcium pump is the sole system responsible for the extrusion of calcium ions. The plasma membrane Ca2+-ATPase (PMCA) is a ubiquitously expressed protein, and more than 26 transcripts of four PMCA genes are distributed in a tissue specific manner. Differences in the structure and localization of PMCA variants are thought to correlate with specific regulatory properties and may have consequences for proper cellular Ca2+ signaling. The regulatory mechanisms of calcium pump activity have been studied extensively, resulting in a new view of the functioning of this important molecule in the membranes.

4

Relationship Between Depression and Strength Training in Survivors of the Ischemic Stroke

100%

Aidar F. J., Gama de Matos D., Jacó de Oliveira R., Carneiro A. L., Tinôco Cabral B. G. d. A., Moreira Silva Dantas P., Machado Reis V.

Journal of Human Kinetics

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2014

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vol. 43

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issue 1

7-15

EN

The Cerebral Vascular Accident is responsible for a significant increase in the mortality rate in individuals who have suffered this condition, regardless of the level of subsequent disability. This study aimed to analyze the influence of a strength training program on indicators of depression in survivors of the ischemic stroke. The study sample included subjects from both genders who were divided into two groups: an experimental group (EG) consisting of 11 subjects aged 51.7 [...] 8.0 years, and a control group (CG) consisting of 13 subjects aged 52.5 [...] 7.7 years. The EG underwent 12 weeks of strength training. Assessment was made in the pre-test before training and at the re-test after 12 weeks of training. We used the Beck Depression Inventory and evaluated 1RM. Significant differences in depression were found between post-test and pretest measurements (Δ% = -21.47%, p = 0,021) in the EG; furthermore, there were significant differences in all indicators of depression between the EG and CG after completing 12 weeks of training. There were significant gains in strength of the EG in relation to the CG. There was a negative correlation between the strength gains as determined with the 1RM test and the levels of depression, especially in lower-limb exercises. The results of this study suggest that improvements in strength are negatively correlated with levels of depression. Improvements in strength are therefore associated with a reduction in levels of depression.

5

Potassium channels in brain mitochondria

100%

Bednarczyk P.

Acta Biochimica Polonica

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2009

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vol. 56

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issue 3

385-392

EN

Potassium channels are the most widely distributed class of ion channels. These channels are transmembrane proteins known to play important roles in both normal and pathophysiological functions in all cell types. Various potassium channels are recognised as potential therapeutic targets in the treatment of Parkinson's disease, Alzheimer's disease, brain/spinal cord ischaemia and sepsis. In addition to their importance as therapeutic targets, certain potassium channels are known for their beneficial roles in anaesthesia, cardioprotection and neuroprotection. Some types of potassium channels present in the plasma membrane of various cells have been found in the inner mitochondrial membrane as well. Potassium channels have been proposed to regulate mitochondrial membrane potential, respiration, matrix volume and Ca+ ion homeostasis. It has been proposed that mitochondrial potassium channels mediate ischaemic preconditioning in various tissues. However, the specificity of a pharmacological agents and the mechanisms underlying their effects on ischaemic preconditioning remain controversial. The following potassium channels from various tissues have been identified in the inner mitochondrial membrane: ATP-regulated (mitoKATP) channel, large conductance Ca2+-regulated (mitoBKCa) channel, intermediate conductance Ca2+-regulated (mitoIKCa) channel, voltage-gated (mitoKv1.3 type) channel, and twin-pore domain (mitoTASK-3) channel. It has been shown that increased potassium flux into brain mitochondria induced by either the mitoKATP channel or mitoBKCa channel affects the beneficial effects on neuronal cell survival under pathological conditions. Recently, differential distribution of mitoBKCa channels has been observed in neuronal mitochondria. These findings may suggest a neuroprotective role for the mitoBKCa channel in specific brain structures. This minireview summarises current data on brain mitochondrial potassium channels and the efforts to identify their molecular correlates.

6

SIGNAL DETECTION APPROACH IN MODELING CONSCIOUSNESS – EMOTION INTERACTIONS

100%

Szczepanowski R.

Acta Neuropsychologica

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2017

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vol. 15(1)

89-96

EN

Contemporary cognitive science attempts to provide computational models that describe how consciousness and emotion constitute adaptive behavior. Given the recent neurobiological view that highlights the fact that the cognitive and emotional regions of the brain work together to achieve conscious behavior, it was shown that signal-detection theory (SDT) can effectively capture the notion of the consciousness–emotion interactions that underlie emotional experience. In particular, I have demonstrated that the hierarchical SDT model is capable of estimating different levels of the hierarchical organization of emotional experience. I have also shown that the threshold SDT model predicts that the formation of emotion experience requires a discrete decision space, which implies that the neural representations of emotion are mediated by thresholds to be experienced consciously. The application of both computational SDT models seems to be a promising advance for studying consciousness–emotion interactions.

7

Integrated self system: a microgenetic approach

88%

Pąchalska M.

Acta Neuropsychologica

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2019

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vol. 17(4)

349-393

EN

This article is dedicated to my beloved mother, Zofia Kuzak, Honorary Member of the Polish Neuropsychological Society, and my highest moral authority, to honor her 100 th birthday. During the Nazi occu pation, at the age of 23, she was deport ed to Germany and forced into slave labour at a German camp, from which she managed to escape. During this escape she had to sit for three long days high up in a tree, without food and without anything to drink, something made possible by her strong physical condition. After three days, she dared to leave the tree and, in throwing the Nazis pursuing her, she ran away not to the South - to her home in Nowy Sącz, but to the North – to Poznań, where she took refuge in the apartment of other relatives, true Polish patriots. She stayed there for the years 1943–1947, keeping the accounts at the large family grocery store. The experiences from this period influenced the formation of her own self and her identity. Her stories about times of tragedy and her ways of dealing with the darkest moments in her life contributed to the fact that I became interested in the subject of the self and identity. I have prepared two monographs and several articles on this topic. This article presents a new approach to integrated self system, associated not only with the physical organism, but also with the social and cultural world. The foundation of this approach to the self is microgenetic theory, especially its account of consciousness, of the transition from self to image, act and object, the epochal nature of this transition, and its relation to introspection, imagination and agency. The affinities of microgenetic theory to many aspects of the thought process should be evident to readers of this journal, but the theory, which was developed from studies of pathological cases, rests on a wealth of clinical detail. In brief, the micro-temporal transition from archaic to recent formations (distributed systems) in the phyletic history of the forebrain constitutes the absolute mental state, with consciousness the relation of self to image and/or object. The reader will be able also to find here the overlapping of states, the continuity of the core over successive states, and subjective time experience. However, the integrated self system is associated not only with the operation of the biological brain and its complex patterns of neural connections, but also with the activity of the social mind/brain, in terms of bonds created within social groups, as well as the cultural mind/brain creating the world of cultural values, including religious ones. I will sum up with a model of self system changing in time (4D), pulsating according to the states of mind (5D) forming different numbers of “bits” of information, as marked on the x axis, and linked to the duration of memories, marked on the y axis. The self system also depends on gravity (6D), and other hyperspace dimensions hitherto unknown in neuroscience.

8

On the other hand: the costs and benefits of left-handedness

75%

Fritsche S. A., Lindell A. K.

Acta Neuropsychologica

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2019

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vol. 17(1)

69-86

EN

Left-handers have been persecuted by right-handers for millennia. This right bias is evident cross-culturally, linguistically (right is literally and figuratively ‘right’, with lefties being described as ‘gauche’, ‘sinister’ and ‘cack-handed’), and environmentally (e.g., equipment design, including power tools, ticket machines, and lecture-room desks). Despite this, the proportion of left-handers has remained constant at approximately 10% of the hominid population, implying that though there are costs associated with left-handedness (if there were not, the proportions of left- and right-handers would be 50:50), left handers must also enjoy fitness advantages that maintain the genes for left-handedness in the population. This paper reviews the costs and benefits of being left-handed, exploring research examining the effects of handedness on brain structure, cognitive function, and human behaviour. The research confirms a variety of left-hander advantages, including some cognitive superiorities, higher wages, and greater sporting and fighting prowess. On the other hand, left-handedness is also associated with significant fitness costs, including an increased risk of accidents, higher substance abuse susceptibility, and earlier death, in comparison with right-handers. In sum, left-handedness confers both costs and benefits, with the latter outweighing the former, maintaining the genes for left-handedness in the population.

63%

Kalinowska A., Kułak W.

Physiotherapy

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2010

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vol. 18

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issue 4

77-82

PL

Poniższy artykuł poświęcony jest zagadnieniom oddziaływania muzyki na ludzki organizm. Celem pracy jest przytoczenie przykładów badań z lat 2000-2010, które wskazują na jej leczniczy wpływ na stan fizyczny i emocjonalny człowieka. Przedstawiono prace poruszające wpływ muzyki w zespole Retta, padaczce, plastyczności mózgu, krążeniu mózgowym, zaburzeniach zachowania i śnie. Ponadto naukowcy wskazują, które obszary mózgowia ulegają aktywacji podczas słuchania muzyki, a także opisują zachowanie się czynności bioelektrycznej mózgu w trakcie ekspozycji na bodziec dźwiękowy.

EN

This article presents the effect of music on human body and contains a review of papers from the last decade, which have confirmed therapeutic effect of music on the physical and emotional condition of patients. The papers cited in the review describe the impact of music in the therapy of Retts syndrome, epilepsy, brain malleability, cerebral circulation, behavioural and sleep disorders. Moreover, scientist indicate, which areas of brain become activated when listening to music and describe bioelectrical behaviour of brain during exposure to sonic stimulus.

15

Tenocyclidine treatment in soman-poisoned rats - intriguing results on genotoxicity versus protection

63%

Petek M. J., Berend S., Kopjar N., Želježić D., Mladinić M., Radić B., Vrdoljak A. L.

Acta Biochimica Polonica

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2008

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vol. 55

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issue 1

97-106

EN

This study aimed to evaluate the antidotal potency of tenocyclidine (TCP) that probably might protect acetylcholinesterase (AChE) in the case of organophosphate poisoning. TCP was tested alone as a pretreatment or in combination with atropine as a therapy in rats poisoned with ¼ and ½ of LD50 of soman. Possible genotoxic effects of TCP in white blood cells and brain tissue were also studied. Results were compared with previous findings on the adamantyl tenocyclidine derivative TAMORF. TCP given alone as pretreatment, 5 min before soman, seems to be superior in the protection of cholinesterase (ChE) catalytic activity in the plasma than in brain, especially after administration of the lower dose of soman. Plasma activities of the enzyme after a joint treatment with TCP and soman were significantly increased at 30 min (P < 0.001) and 24 h (P = 0.0043), as compared to soman alone. TCP and atropine, given as therapy, were more effective than TCP administered alone as a pretreatment. The above therapy significantly increased activities of the enzyme at 30 min (P = 0.046) and 24 h (P < 0.001), as compared to controls treated with ¼ LD50 of soman alone. Using the alkaline comet assay, acceptable genotoxicity of TCP was observed. However, the controversial role of TCP in brain protection of soman-poisoned rats should be studied further.

16

Zawartość 5-hydroksytryptaminy w mózgu szczurów z równoczesną lezją ośrodkowego układu dopaminergicznego i noradrenergicznego

63%

Nowak P., Niwiński J., Kőrössy E., Drab J., Walawender I., Bojanek K., Szkilnik R., Brus R.

Annales Academiae Medicae Silesiensis

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2009

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vol. 63

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issue 4

39-45

EN

BACKGROUND Rats lesioned shortly after birth with 6-OHDA (neurotoxin for the central dopaminergic system) have been proposed to be a near-ideal model of severe Parkinson’s disease, because of non-lethality of the procedure, near-total destruction of nigrostriatal dopaminergic fi bres and near-total dopamine (DA) denervation of striatum. In such rodent model of Parkinson’s disease increase of serotoninergic system in the brain of adult rats was observed. The aim of presented study was to examine the central serotoninergic system in adult rats simultaneously lesioned with central dopaminergic (using 6-OHDA) and noradrenergic system (using DSP-4). MATERIAL AND METHODS Newborn male Wistar rats were injected on the day 1st and 3rd of life with DSP-4 (neurotoxin for noradrenergic system) 50.0 mg/kg SC, and on the day 3rd with 6-OHDA 134 μg ICV. Separately and concomitantly. In adult animals the level of biogenic amines in the brain was estimated by HPLC/ED technique. RESULTS It was shown that in rats lesioned as neonates with 6-OHDA increase of 5-HT and its metabolite 5-HIAA was observed in the brain of adult rats. Simultaneous lesion of the central dopaminergic and noradrenergic system induce further increase in the level of indole amines in the brain of adult rats. CONCLUSIONS Simultaneous lesion of the central dopaminergic and noradrenergic system of rats as neonates increased activity of the central serotoninergic system which seems to be a substitute of the dopaminergic one.

PL

WSTĘP 6-OHDA, neurotoksyna ośrodkowego układu dopaminergicznego podana szczurzym noworodkom wywołuje trwałe uszkodzenie powyższego układu utrzymujące się przez całe życie zwierzęcia, które uznawane jest za zwierzęcy model choroby Parkinsona. Towarzyszy temu wzrost aktywności ośrodkowego układu serotoninergicznego. Celem niniejszych badań była ocena zmian układu serotoninergicznego u szczurów z równoczesną lezją ośrodkowego układu dopaminergicznego (podaniem 6-OHDA) oraz noradrenergicznego podaniem DSP-4 (neurotoksyny układu noradrenergicznego) . MATERIAŁ I METODY Szczurzym noworodkom samcom szczepu Wistar podano 1-go i 3-go dnia życia DSP-4 50.0 mg/kg SC oraz 3-go dnia życia 6-OHDA 134 μg ICV oddzielnie lub łącznie. U dorosłych zwierząt oznaczono zawartość amin biogennych w mózgu metodą HPLC/ED. WYNIKI Wykazano i potwierdzono, że u dorosłych szczurów z lezją ośrodkowego układu dopaminergicznego wykonaną w okresie noworodkowym dochodzi do wzrostu zawartości 5-HT i 5-HIAA w mózgu dorosłych szczurów. Równoczesna lezja ośrodkowego układu noradrenergicznego wykonana podaniem noworodkom DSP-4 powoduje dalszy wzrost zawartości badanych amin indolowych w mózgu dorosłych szczurów. WNIOSKI: Łączne podanie 6-OHDA i DSP-4 (neurotoksyny układu dopaminergicznego i noradrenergicznego) noworodkom powoduje nasilenie aktywności ośrodkowego układu serotoninergicznego u dorosłych szczurów, który wydaje się zastępować niedoczynny układ dopaminergiczny.

17

Aktualne poglądy na temat roli witaminy D w patogenezie stwardnienia rozsianego

63%

Antczak M., Głąbiński A.

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2013

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vol. 13

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issue 1

24-30

EN

Vitamin D is commonly known for its role in calcium-phosphate metabolism but there is growing amount of data showing its pleiotropic actions. Positive correlation between vitamin D deficiency and the prevalence of autoimmune diseases including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, etc. has been observed. Vitamin D receptors have been found in spectrum of tissues and organs, including bones, muscles, reproductive organs, heart, brain, and within the immune system. Widely investigated immunomodulatory action of vitamin D affects both innate and adaptive immunity by suppressing T cell proliferation and cytotoxity, promoting regulatory T cells differentiation and modulating macrophage and dendritic cell functions. Multiple sclerosis (MS) is an autoimmune disease of the central nervous system caused by complex and predominantly unknown interactions of genetic susceptibility and environmental factors. Epidemiological studies show that the sun exposure and corresponding vitamin D level are important factors that can explain geographical distribution of MS. Some preliminary observations suggest that vitamin D supplementation not only reduces the risk of developing MS but also modulates disease course and reduces relapses rate among patients with relapsing-remitting MS. Further studies and clinical trials are required to confirm the role of vitamin D in MS pathogenesis.

PL

Witamina D jest powszechnie znana ze swojej roli w gospodarce wapniowo-fosforanowej, ale wzrastająca ilość danych wskazuje na jej działania plejotropowe. Zaobserwowano pozytywną korelację między niedoborem witaminy D a występowaniem chorób autoimmunologicznych, w tym stwardnienia rozsianego, reumatoidalnego zapalenia stawów, tocznia rumieniowatego układowego itp. Receptory witaminy D są obecne w szeregu tkanek i narządów, w tym w kościach, mięśniach, narządach rozrodczych, sercu, mózgu oraz w obrębie układu odpornościowego. Coraz lepiej poznawane działanie immunomodulujące witaminy D obejmuje wpływ zarówno na mechanizmy odporności wrodzonej, jak i adaptacyjnej, poprzez hamowanie proliferacji i cytotoksyczności limfocytów T, promowanie różnicowania limfocytów T regulatorowych oraz modulowanie działania makrofagów i komórek dendrytycznych. Stwardnienie rozsiane (łac. sclerosis multiplex, SM) jest chorobą autoimmunologiczną ośrodkowego układu nerwowego spowodowaną przez skomplikowane i w dużej mierze nieznane interakcje między predyspozycjami genetycznymi i czynnikami środowiskowymi. Badania epidemiologiczne wskazują, że ekspozycja na promieniowanie słoneczne i związany z nią poziom witaminy D są ważnymi czynnikami mogącymi wyjaśniać zróżnicowanie geograficzne częstości zachorowań na SM. Wyniki niektórych wstępnych obserwacji sugerują, że suplementacja witaminy D może zmniejszać ryzyko zachorowania na SM oraz modulować przebieg choroby i zmniejszać częstość jej nawrotów u pacjentów z rzutowo-remisyjną postacią SM. Wyniki te skłoniły do podjęcia prób włączenia witaminy D jako składnika wspomagającego terapię SM. Obserwacje te wymagają dalszego potwierdzenia i badań klinicznych.

18

Effect of chlorpheniramine and cimetidine, a histamine H1 and H2 antagonist on (3H)glucose uptake in the brain of adult rats lesioned with 5,7-dihydroxytryptamine as neonates

51%

Jośko J., Drab J., Nowak P., Szkilnik R., Boroń D., Elwart M., Konecki J., Brus H., Brus R.

Annales Academiae Medicae Silesiensis

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2012

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vol. 66

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issue 2

13-19

EN

BACKGROUND The aim of the study was to examine eff ect of chlorpheniramine (hista- mine H1 receptor antagonist) and cimetidine (histamine H2 receptor an- tagonist) on (3H)glucose uptake in the brain of adult rats lesioned with 5,7-dihydroxytryptamine (neurotoxin for the central serotoninergic sys- tem) as neonates. MATERIAL AND METHODS Male 3-days old Wistar rats were injected with serotoninergic neurons neurotoxin 5,7-dihydroxytryptamine, 75 μg icv. Control rats were injected with saline 10 μg icv. At 8 weeks level of 5-HT and 5-HIAA was estimat- ed in the striatum, frontal cortex and hippocampus of the brain. Other 8 weeks old animals of control and 5,7-DHT lesioned as neonates were injected with S(+)chlorpheniramine (H1 receptor antagonist) 10.0 mg/kg ip or with cimetidine (H2 receptor antagonist) 5.0 mg/kg ip. Control rats were injected with saline 1.0 ml/kg ip. 60 minutes later 6-(3H)-D-glucose was applied in a dose of 500 μCi/kg ip and 15 minutes later all rats were decapitated and their brains were excised, placed on the ice and sample of frontal cortex, striatum, hippocampus, thalamus with hypothalamus, pons and cerebellum were separated and weighted. Then in the examined tissues radioactivity was measured in liquid scintillation counter and ex- pressed in DPM/100 mg of wet tissue. RESULTS 5,7-DHT decreased signifi cantly the level of 5-HT and 5-HIAA in all examined tissues in the brain of adult rats. In rats neonatally lesioned with 5,7-DHT radioactivity signifi cantly increased as compare to the control. Chlorpheniramine prevent signifi cantly that eff ect in the frontal cortex and cimetidine in the frontal cortex, hippocampus and cerebellum. CONCLUSION From above we conclude that in the brain of mammalians the metabolic link between histaminergic and serotoninergic system exist in regulation of energetic prcesses connected with glucose metabolism.

PL

WSTĘP Celem pracy było zbadanie wpływu chlorfeniraminy, antagonisty receptora histaminowego H1 i cymetydyny, antagonisty receptora histaminowego H2 na wychwyt (3H)glukozy w mózgu dorosłych szczurów z lezją (zniszczenie) ośrodkowego układu serotoninergicznego wywołaną podaniem noworodkom neurotoksyny 5,7-dihydroksytryptaminy. MATERIAŁ I METODY Trzydniowe noworodki płci męskiej szczepu Wistar otrzymały do bocznej komory mózgu (icv) 75 μg 5,7-dihydroksytryptaminy (5,7-DHT), neurotoksynę układu serotoninergicznego. Zwierzęta kontrolne otrzymały icv 10 μl 0,9% roztworu NaCl. Po osiągnięciu 8 tygodni życia zwierzęta dekapitowano i w korze czołowej, prążkowiu oraz zakręcie hipokampa oznaczono zawartość 5-HT i 5-HIAA metodą HPLC/ED. Osobnej grupie badanej i kontrolnej podano S(+)chlorfeniraminę 10,0 mg/kg ip (antagonista receptora histaminowego H1) lub cymetydynę 5,0 mg/kg ip (antagonista receptora histaminowego H2). Zwierzęta kontrolne obu grup otrzymały 0,9% roztwór NaCl 1,0 ml/kg ip. Po 60 minutach wszystkie szczury otrzymały 6-(3H)-D-glukozę 500 μCi/kg ip. Po dalszych 15 minutach zwierzęta dekapitowano, wyjmowano z czaszki mózg, separowano z niego korę czołową, prążkowie, hipokamp, wzgórze z podwzgórzem, most i móżdżek, w których oznaczono radioaktywność przy użyciu licznika scyntylacyjnego. Wyniki wyrażono w DPM (Desintegrations Per Minute) na 100 mg świeżej tkanki. WYNIKI 5,7-DHT podany noworodkom znamiennie obniżył zawartość 5-HT i 5-HIAA w badanych fragmentach mózgu dorosłych szczurów. U zwierząt z lezją ośrodkowego układu serotoninergicznego we wszystkich badanych częściach mózgu wykazano znamienny wzrost wychwytu (3H)glukozy. Badani antagoniści receptorów histaminowych nie wpływali na wychwyt (3H)glukozy w mózgu zwierząt grupy kontrolnej, natomiast chlorfeniramina zapobiegała wychwytowi glukozy tylko w korze mózgowej, a cymetydyna w korze mózgowej, hipokampie i móżdżku zwierząt z lezją ośrodkowego układu serotoninergicznego wywołaną podaniem noworodkom 5,7-DHT. WNIOSKI Wyniki wskazują na metaboliczne powiązania w mózgu ssaków między układem serotoninergicznym i histaminergicznym.

19

Czego dowiedzieliśmy się o ADHD dzięki czynnościowym badaniom neuroobrazowym?

51%

Dąbkowska M.

Psychiatria i Psychologia Kliniczna

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2010

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vol. 10

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issue 3

195-199

EN

Functional imaging techniques provide information about metabolic activity and neural signalling in populations of neurons. Brain activation in ADHD has been assessed using a variety of techniques. The studies have been conducted in resting subjects and under varying conditions of cognitive stress. The aim of this article is to review the neuroimaging literature in ADHD, mainly in functional magnetic resonance imaging, positron emission tomography and single photon emission tomography. Through the use of various functional imaging techniques in conjunction with behavioural data and lesion studies we are now able to learn not only about the function of a brain region, but also about the use of covert behavioural and cognitive strategies. The impaired flexibility in recruiting brain regions and associated strategies limit adaptation to new cognitive demands as they present and may require more effort in processing. This article presents findings suggesting that ADHD should be characterized not only by neural hypoactivity, but neural hyperactivity as well, in regions of the brain that may relate to compensatory brain and behavioural functioning. The frontostriatal dysfunction may be central to the pathophysiology of ADHD, but there is now substantial evidence of functional alterations in regions outside the frontostriatal circuitry in ADHD, most notably in the cerebellum and the parietal lobes. More research is needed to elucidate the nature of contributions of nonfrontostriatal regions to the pathophysiology of ADHD.

PL

Czynnościowe badania neuroobrazowe dostarczają informacji o aktywności metabolicznej i przewodzeniu neuronalnym. W ocenie aktywności mózgu u osób z ADHD (attention-deficit/hyperactivity disorder, ADHD) stosowano różne techniki. Przeprowadzono badania w spoczynku i podczas wykonywania testów poznawczych. Celem pracy jest przegląd literatury na temat wyników badań neuroobrazowych w ADHD, szczególnie z wykorzystaniem czynnościowego rezonansu magnetycznego, tomografii emisji pozytronowej, tomografii pojedynczego fotonu. Za pomocą różnorodnych technik czynnościowego obrazowania stosowanych podczas zadań behawioralnych lub u osób z uszkodzeniem funkcji można uzyskać informacje nie tylko o roli obszarów mózgu, ale i o dotychczas nieznanych strategiach zachowania i funkcji poznawczych. Osłabione zdolności przystosowawcze we włączaniu poszczególnych regionów mózgu i związane z tym trudności adaptacyjne do nowych wymagań poznawczych wymuszają większy wysiłek podczas procesów przetwarzania. Zawarte w artykule informacje sugerują, że ADHD charakteryzuje się osłabioną aktywnością neuronalną oraz nadaktywnością – zwłaszcza tych obszarów mózgu, które mogą pełnić rolę kompensującą i wyrównującą utrudnione funkcjonowanie osób z ADHD. Głównym podłożem ADHD mogą być nieprawidłowości w aktywności połączeń korowo-prążkowiowych, niemniej jednak jest coraz więcej danych o zaburzeniach w innych lokalizacjach, takich jak móżdżek i płaty ciemieniowe u osób z ADHD. Potrzebne są dalsze badania czynnościowe w celu wyjaśnienia roli innych regionów poza siecią połączeń czołowo-prążkowiowych w patofizjologii ADHD.

20

Czego dowiedzieliśmy się o ADHD dzięki strukturalnym badaniom neuroobrazowym?

51%

Dąbkowska M.

Psychiatria i Psychologia Kliniczna

|

2010

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vol. 10

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issue 3

200-204

EN

Attention-deficit/hyperactivity disorder (ADHD) belongs to the most common behavioural disorders of childhood. ADHD can be conceptualised as a diverse developmental disorder characterised by a variable clinical expression, which is underlain by heterogeneity leading to the neural system dysfunction. Neuroimaging for childhood psychiatric disorders has the potential to increase our understanding of the pathophysiology of childhood mental disorders. In recent years, neuroimaging techniques have been used with increasing frequency in attempts to identify structural and functional abnormalities in the brains of children with ADHD. Structural imaging methods have localized abnormalities in key brain regions and neural networks associated with cognition and behaviour consistent with the clinical picture of ADHD. Structural imaging studies suggest that the ADHD pathophysiology would be conditioned by the dysfunction in frontosubcortical pathways. Currently increasing is the evidence that other brain regions such as the cerebellum, the parietal lobes and temporal lobes may also have an important role in this condition. The findings generally suggest deficits in the brain areas mentioned above, with decreased volumes. However, it is also evident that some areas show enlargement as a compensation for the observed deficits. Apart from the issue of reliability, there is a more basic question about how the results of neuroimaging studies are to be interpreted.

PL

Zaburzenie hiperkinetyczne (attention-deficit/hyperactivity disorder, ADHD) należy do najczęściej obserwowanych zaburzeń behawioralnych okresu dzieciństwa. Może być rozpatrywane jako zróżnicowane zaburzenie rozwojowe, charakteryzujące się różnorodną ekspresją kliniczną, u podłoża którego leżą różne czynniki prowadzące do dysfunkcji systemu nerwowego. Badania neuroobrazowe u pacjentów z zaburzeniami psychicznymi wieku rozwojowego przyczyniają się do przybliżenia wyjaśnienia patofizjologii zaburzeń psychicznych u dzieci. W ostatnich latach obserwuje się znaczący wzrost częstości wykorzystania techniki neuroobrazowania do identyfikacji odchyleń w mózgu dzieci z zaburzeniem hiperkinetycznym. Strukturalne badania neuroobrazowe pokazują nieprawidłowości w okolicach mózgu i sieci połączeń kluczowych, które mogą być podłożem objawów ADHD, takich jak zaburzenia uwagi i behawioralne. Wyniki tych badań sugerują dysfunkcje połączeń czołowo-podkorowych jako podłoże patofizjologii ADHD. Obecnie wzrasta liczba doniesień o roli innych regionów mózgu, takich jak móżdżek, płaty ciemieniowe i skroniowe w etiologii tego zaburzenia. Wskazuje się głównie na deficyty we wspomnianych regionach, spadek objętości. Niektóre prace mówią o powiększeniu części obszarów mózgu jako kompensacji obserwowanych deficytów. Odkładając na bok brak jednoznacznych wyników uzyskanych za pomocą neuroobrazowania, należy zastanowić się nad ich interpretacją.

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Czego dowiedzieliśmy się o ADHD dzięki czynnościowym badaniom neuroobrazowym?

Czego dowiedzieliśmy się o ADHD dzięki strukturalnym badaniom neuroobrazowym?