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1

Look away: neural correlates for suppression of the visual grasp reflex in the anti-saccade task

100%
Everling S.
Acta Neurobiologiae Experimentalis
|
2005
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tom 65
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nr 5
2

Neural control of probabilistic motor learning

100%
Ashe J.
Acta Neurobiologiae Experimentalis
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2005
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tom 65
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nr 5
3

Neural correlates of perceptual and movement decisions in monkey prefrontal cortex

100%
Acuna C.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
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nr 5
4

Role of prefrontal cortex and ventral striatum in guidance of instrumental behaviour by expected reward

100%
Hauber W.
Acta Neurobiologiae Experimentalis
|
2005
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tom 65
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nr 5
5
Content available remote

Corticotropin releasing factor receptor 1 antagonist differentially inhibits freezing behavior and changes gamma-aminobutyric acid-ergic activity in the amygdala in low- and high-anxiety rats

84%
Skorzewska A., Wislowska-Stanek A., Lehner M., Turzynska D., Sobolewska A., Krzascik P., Plaznik A.
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 1
6
Content available remote

The impact of 3,4-methylendioxymethamphetamine (MDMA) abstinence on seeking behavior and the expression of the D2-like and MGLU5 receptors in the rat brain using saturation binding analyses

84%
Frankowska M., Miszkiel J., Pomierny-Chamiolo L., Pomierny B., Celeste Borelli A., Suder A., Filip M.
Journal of Physiology and Pharmacology
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2020
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tom 71
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nr 4
7

Glia and glutamate: new key players in the pathology of major depression

84%
Rajkowska G.
Acta Neurobiologiae Experimentalis
|
2009
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tom 69
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nr 3
Postmortem studies in depression reveal age-dependent cell pathology in prefrontal cortex. Prominent reductions in glia and specifi cally, in astrocytes, are observed in younger depressed, whereas neuronal pathology is found in elderly with depression. As astrocytes regulate extracellular concentrations of glutamate (via glial glutamate transporters), an early defi cit in astrocytes could lead to increases in extracellular glutamate and toxic damage to neurons as depression progresses. This is supported by postmortem studies of reduced expression of mRNA and protein for the glial glutamate transporter in younger depressed and by reductions in glutamatergic neurons in elderly depressed. Moreover, alterations in glutamate metabolism are reported in neuroimaging studies of depressed patients. Interestingly, agents increasing expression of glial glutamate transporters and/or altering glutamate neurotransmission show antidepressant activity. Our hypothesis that glial pathology is an initial stage of cellular and neurochemical changes in depression was confi rmed by observations of glial/glutamate defi cits in chronically stressed rodents. Pharmacologically-induced loss of astroglia, but not neurons in the rat prefrontal cortex will induce depressive-like behaviors. Moreover, treatment with riluzole (a modulator of glutamate release) reverses stress-induced depressive-like behaviors and blocks glia impairments providing a link between dysfunction of glia and glutamate in depression.
8
Content available remote

Intraperitoneal zinc administration increases extracellular zinc in the rat prefrontal cortex

84%
Opoka W., Sowa-Kucma M., Kowalska M., Bas B., Golembiowska K., Nowak G.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 3
477-487
Single administration of zinc evokes pharmacological behavioral effects in rodents, while no brain zinc alterations were detected. The aim of the present study was to examine the effect of a single zinc hydroaspartate intraperitoneal (ip) administration on the extracellular (synaptic) zinc concentration in the rat prefrontal cortex. We used anodic stripping voltammetric (ASV) method of zinc determination in microdialysate, which assays the extracellular zinc concentration. We report that acute (65 mg/kg) zinc hydroaspartate administration (ip) increases the extracellular zinc by 48% in the rat prefrontal cortex. These data for the first time demonstrate: 1) utility of ASV zinc detection in brain microdialysates and 2) that single ip zinc administration increases brain (cortical) extracellular zinc pool. The results indicate zinc-induced fast brain penetration and may explain its rapid pharmacological effects.
9
Content available remote

Prefrontal control of respiration

84%
Aleksandrov V. G., Ivanova T. G., Aleksandrova N. P.
Journal of Physiology and Pharmacology. Supplement
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2007
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tom 58
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nr 5
10
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Content available

Cortical localization of dopamine D4 receptors in the rat brain - immunocytochemical study

84%
Wedzony K., Chocyk A., Mackowiak M., Fijal K., Czyrak A.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 2
11

Degeneration of astrocytes in the prefrontal cortex induces depressive-like behavior in rats: Behavioral, immunochemical and histological studies

67%
Smialowska M., Szewczyk B., Wawrzak-Wlecial A., Domin H.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Postmortem studies of depressed patients showed that one of the most consistent findings is a decrease in the density of glial cells in human brain cortical regions, especially in the prefrontal and cingular areas. Furthermore, a decline in the number of astrocytes in the prefrontal cortex was found in rats after chronic unpredictable stress – one of the generally accepted animal models of depression. An important function of astrocytes in the brain tripartite synapse is the uptake of released glutamate. Hence the basic consequence of the loss of astrocytes is a reduction in glutamate uptake and an excess of glutamate in the synaptic cleft. The glutamatergic predominance in the excitator-inhibitory balance is postulated to be involved in the pathogenesis of depression. Recently, depressive-like behavior have been demonstrated in rats after astrocytes ablation. Therefore in the present study we tried to ascertain whether astroglial degeneration in the prefrontal cortex was sufficient to induce a depressive-like behavior and could serve as an animal model of depression. Astrocytic toxin L- or D,Lalpha-aminoadipic acid (AAA), 100 µg/2 µl, was microinjected bilaterally into rat medial prefrontal cortex (PFC). The toxins were injected twice, on day 1 and 2; afterwords depressive-like behavior was assessed by a forced swim test on day 5 of the experiment. Some rats were additionally treated with the antidepressant imipramine (30 mg/kg, i.p.) 24, 5 and 1 h before the forced swim test. The rats’ brains were taken out for an analysis on day eight. Histological verifications of the injection sites and immunohistochemical staining for the astrocytic marker glial fibrillary acidic protein (GFAP), were carried out. The GFAP positive cells were stereologically counted in the PFC. Also the level of GFAP expression was determined by the Western blot analysis in all the experimental groups. It was found that both L-AAA and DL-AAA induced a significant increase in immobility time in the forced swim test, without changing the overall locomotor activity, which indicates depressive-like effects of these compounds. The immunohistochemical and Western blot analyses showed a significant decrease in the number of GFAP-positive cells and GFAP level in the PFC of toxin-treated rats. The decrease amounted to ca. 50%. Both the behavioral and the GFAP changes were reversed or partially inhibited by imipramine injection. The obtained results suggest an important role of astrocytes in the PFC in mood regulation; moreover, they indicate that the degeneration of astrocytes in this structure may be used as an animal model of depression. This study was supported by Grant POIG.01.01.02-12-004/09Friday, November 23, 2012
12
Content available remote

Chronic stress adaptation of the nitric oxide synthases and IL-1beta levels in brain structures and hypothalamic-pituitary-adrenal axis activity induced by homotypic stress

67%
Gadek-Michalska A., Tadeusz J., Rachwalska P., Bugajski J.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 3
13
Content available remote

Complex estrogenic regulation of catechol-O-methyltransferase (COMT) in rats

67%
Schendzielorz N., Rysa A., Reenila I., Raasmaja A., Mannisto P. T.
Journal of Physiology and Pharmacology
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2011
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tom 62
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nr 4
14

Prefrontal catecholaminergic turnover and antioxidant defense system of chronically stressed rats

67%
Popovic N., Pajovic S. B., Stojiljkovic V., Pejic S., Todorovic A., Pavlovic I., Gavrilovic L.
Folia Biologica
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2017
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tom 65
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nr 1
15

Dopaminergic innervation of the brain in pigeons. The presumed prefrontal cortex

67%
Divac I., Thibault J., Skageberg G., Palacios J. M., Dietl M. M.
Acta Neurobiologiae Experimentalis
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1994
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tom 54
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nr 3
16

Catecholamines and DOPAC in cortical and neostriatal regions during rats learning of delayed alternation

67%
Mogensen J., Bjorklund A., Divac I.
Acta Neurobiologiae Experimentalis
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1992
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tom 52
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nr 2
17

Retention and relearning of spatial delayed alternation in rats after combined or sequential lesions of the prefrontal and parietal cortex

67%
Wortwein G., Mogensen J., Divac I.
Acta Neurobiologiae Experimentalis
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1993
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tom 53
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nr 2
18

Cortical projections of the thalamic mediodorsal nucleus in the rat. Definition of the prefrontal cortex

67%
Divac I., Mogensen J., Petrovic-Minic B., Zilles K., Regidor J.
Acta Neurobiologiae Experimentalis
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1993
|
tom 53
|
nr 2
19

Behavioural changes after ablation of subdivisions of the rat prefrontal cortex

67%
Mogensen J., Divac I.
Acta Neurobiologiae Experimentalis
|
1993
|
tom 53
|
nr 3
20

Inhibitory control of the defence-aggression reaction including its cardiovascular components

59%
Zbrozyna A. W., Westwood D. M.
Acta Neurobiologiae Experimentalis
|
1993
|
tom 53
|
nr 1
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