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1
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Dopamine, serotonin and noradrenaline changes in the striatum of C57BL mice following myelin oligodendrocyte glycoprotein (MOG) 35-55 and complete Freund adjuvant (CFA) administration

100%
Balkowiec-Iskra E., Kurkowska-Jastrzebska I., Joniec I., Ciesielska A., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
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2007
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vol. 67
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issue 4
379-388
EN
Many data suggest involvement of inflammation in neurodegeneration. However, the exact mechanisms of this cooperation are poorly understood. We have previously shown that induction of inflammatory reaction, both before and after injury of the striatum, affects regeneration of dopaminergic neurons. In the present research we studied the role of inflammatory reaction in non-injured striatum. We used myelin oligodendrocyte glycoprotein (MOG) 35-55 in complete Freund's adjuvant (CFA) to elicit experimental autoimmune encephalomyelitis (EAE) mice model. As determined by HPLC, striatal dopamine (DA) and serotonin levels in mice treated with either MOG 35-55 in CFA or CFA alone were significantly higher compared to vehicle-treated controls on 13th day after induction. The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Noradrenaline (NA) concentration did not differ between groups. Moreover, the striatal mRNA IL-1beta and TNF-alpha levels were elevated during induction phase of EAE in both groups, as determined by RT-PCR. Our data indicate regulatory connection between dopaminergic and immune systems.
2
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Acute hypoxia modulates arachidonic acid metabolism in cat carotid bodies.Role of dopamine

100%
Strosznajder R.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 2
535-543
EN
The hypoxic stimulus of arterial blood is transformed at the carotid body (CB) chemoreceptors into neuronal signals regulating respiration.The mechanism of chemotransduction is until now not well understood.In this study the regulation of arachidonic acid (AA) release and its incorporation into membrane glycerolipids were investigated.Moreover, the effect of hypoxia and dopamine (DA) on these processes was calculated.The CB were excised from cats exposed in situ to normoxia or hypoxia.Then CB were homogeni and used as a source of enzyme (s).It was observed thar Ca2+ enhanced the release of AA by 40-50% through the action of phospholipase C together with diacyl-glycerol lipase and phospholipase A2.Acute hypoxia significantly decreased AA incorporation into phosphatidylinositol (PtdIns) and enhanced the level of AA radioactivity in diacylglycerol and AA-CoA.These results suggest that hypoxia induces inhibition of AA on the level of acyl-CoA-lysophospholipid:acylotransferases.DA decreased AA incorporation into PtdIns and exerted an additive inhibitory effect in hypoxic samples.These results demonstrated that AA metabolism in CB is significantly affected by hypoxia and that DA is not responsible for the hypoxia-induced alteration of lipid metabolism in CB.
3
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D1 dopamine receptors distribution following photothrombotic stroke in rat cerebral cortex

88%
Rogozinska K., Skangiel-Kramska J.
Acta Neurobiologiae Experimentalis
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2005
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vol. 65
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issue 2
167-172
EN
The effect of focal photothrombotic stroke on the distribution of D1 dopamine receptor (D1R) sites was examined in different cortical areas of rat brain with quantitative receptor autoradiography using [3H]SCH23390 as a ligand. Unilateral cortical stroke was located in the primary somatosensory cortex. After different survival times (1, 7 and 28 days) D1R binding levels were determined in the lesion core, penumbra, frontoparietal motor (FrPaM) and somatosensory (FrPaSS) areas as well as in homotopic regions in the contralateral hemisphere. One day after stroke, D1R density decreased by 36% (P<0.01) in the lesion core relative to sham-operated controls. At 7th day binding density was further reduced by 56% (P<0.002). Twenty-eight days after infarction, D1R binding returned to control level. No alterations in D1R binding levels were found in penumbra and other investigated regions. We suggest that the return of D1R binding to control level in the area initially corresponding to the infarct results from the shrinkage of the lesion volume.
4
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Effects of melatonin infused into the III ventricle on prolactin, beta-endorphin and luteotropin secretion in ewes during the different stages of the reproductive cycle

88%
Misztal T., Romanowicz K., Barcikowski B.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 3
769-778
EN
Secretion of all the pituitary hormones undergoes marked circadian and seasonal changes.The rhythmicity of these changes is controled by the circadian pacemaker system and the pineal gland transmitting daylength informatoin to the neuroendocrine axis via the secretion of melatonin.This article presents data on the effects of the short-term melatonin administratoin into the third brain ventricle on prolactin, beta-endorphin and luteotropin secretion in ewes kept under the increasing and decreasing daylenght conditions.Additional emphasis is given to dopamine and LHRH release in the madiobasal hypothalmus under the malatonin treatment by the push-pull method.The long-term and short-term actions of melatonin on the hormonal status in ewes is also discussed.
5
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Effect of acute hepatic encephalopathy on [3H]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2+

88%
Borkowska H., Oja S. S., Hilgier W., Saransaari P., Albrecht J.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 1
1-7
EN
Hepatic encephalopathy (HE) is characterized by motor symptoms associated with disturbed functions of the dopaminergic systems, but the underlying mechanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KCl) -stimulated release of newly loaded [3H]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2+. In the present study we compared the effects of HE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the presence and absence of Ca2+. HE enhanced the KCl-stimulated [3H]dopamine release from striatal and frontal cortical synaptosomes in the presence of Ca2+ to the same extent as in slices prepared from the respective brain regions. In the absence of Ca2+ a slight reduction in dopamine release was observed in frontal cortical synaptosomes from HE rats when compared to control rats, while no effect of HE on the release was discernible in frontal cortical and striatal slices and striatal synaptosomes. We conclude that in both brain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ influx without affecting the release mediated by means of plasma membrane transporters or exocytosis involving intraterminal Ca2+.
6
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In vitro pituitary prolactin, growth hormone and follicle stimulating hormone secretion during sexual maturation of female rats primed with melatonin

75%
Diaz_ R. E., Fernandez_ A. C., Castrillon P. O., Esquifino_ P. A. I., Diaz_ L. B.
Acta Neurobiologiae Experimentalis
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2001
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vol. 61
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issue 1
27-33
EN
The influence of in vivo melatonin administration on in vitro pituitary follicle stimulating hormone (FSH), growth hormone (GH) and prolactin secretion, as well as the possible influence of dopamine (DA) were evaluated in prepubertal (31-day-old), pubertal (33-day-old) and adult female rats at diestrus phase of the sexual cycle. The in vitro pituitary hormone secretions were evaluated at basal rate for the first hour of incubation only, in Krebs Ringer phosphate (KRP) (I1) and after a second hour of incubation with KRP (I2) or with KRP+DA (I2 plus DA). I1PRL secretion was significantly higher in 33-day-old control and melatonin treated (MEL) rats as compared to I2 periods. However, in 31-day-old rats I1 secretion was higher than in the I2 or I2+DA periods, in MEL rats. In vitro GH secretion was significantly higher at I1 than during I2 periods in the control 31- and 33-day-old groups, but not in MEL rats. The only significant effect of DA was the elevation of GH in prepubertal MEL rats. In vitro FSH release was increased by melatonin in 31-and 33-day-old female rats. No differences in PRL, GH and FSH secretion were found in adult rats. In conclusion, the results show that melatonin effects upon in vitro pituitary gland activity are reproductive-stage-dependent modifying the secretory capacity of the lactotrop, gonadotrop and somatotrop during prepubertal and pubertal ages but not in adult rats studied at a quiescent phase of the sexual cycle.
7
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Serotonin 5-HT systems mediate dopamine /DA/ receptor supersensitivity

75%
Kostrzewa R. M., Gong L., Brus R.
Acta Neurobiologiae Experimentalis
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1993
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vol. 53
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issue 1
31-41
EN
To study interactions between DA and 5-HT neurochemical systems in the DA D1 supersensitized induction of oral activity in neonatal 6-hydroxydopamine /6-OHDA/ lesioned rats, the effects of a variety of 5-HT receptor agonists and antagonists were determined.
8
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Neural systems mediating the negative feedback actions of estradiol and progesterone in the ewe

63%
Goodman R. L.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 3
727-741
EN
The ewe shows a marked seasonal variation in the effect of ovarian steroids on pulsatile GnRH secretion.In the breeding season progesterone inhibits GnRH pulse frequency, while estradiol suppresses puilse amplitude.In anestrus, both steriods inhibit pulse frequency.The effects of progestrone in both seasons are mediated by endogenous opioid peptides (EOP) that act in the preoptic area (POA) and medial basal hypothalmus (MBH).However, knife cut studies indicate that actions in the MBH are most important.Moreover, blockade of EOP receptors activates GnRH perikarya in the MBH, but not those in the POA.Thus interactions between EOP and GnRH neurons within the MBH may be critical for progesterone negative feedback.The neural systems mediating estradiol suppression of GnRH pulse amplitude in the breeding season are largely unknown, although alpha-adrenergic neurons nay be involved.The seasonal variation in inhibition of GnRH pulse frequency by estradiol is postulated to be mediated by a group of dopaminergic (DA) neurons that have three important properties: (1)they inhibit GnRH pulse frequency; (2) their activity is stimulated by estradiol; and (3) they are functional in anestrus, but not the breeding season.Recent work examining the effects of lesions of DA neyrone and the ability of estradiol to induce Fos inDA cells srongly suggest that DA neurons in the retrochiasmatic area (A15) and POA (A14) have all three characteristics.We thus propose that these DA neurons are responsible for the seasonal variation in the ability of estradiol to inhibit GnRH pulse frequency.
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