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Magnesium in pathophysiology and therapy of affective disorders

100%

Poleszak E., Nowak G.

Journal of Elementology

2006

tom 11

nr 3

p.389-397,fig.,ref.

Magnesium possesses activity in a broad range of biochemical processes in living organisms. This review focus on the role of magnesium in pathophysiological and therapeutical mechanisms of affective disorders. Magnesium as an antagonist of the N-methyl-D- -aspartate (NMDA)/glutamate receptor complex, is active in the antidepressant screen test, forced swim test in rodents. Clinical studies, although providing very limited amount of data, suggest possible efficacy of magnesium in mania (bipolar affective disorders). Magnesium deficiency induced depression-like behavior in animals, and such an effect in humans is also suggested. All the available data indicate the importance of magnesium homeostasis in pathophysiology and therapy of affective disorders.

The influence of imipramine and pramipexole on depressivelike behaviour in an animal model of a pre-clinical stage of Parkinson’s disease

100%

Berghauzen K., Wardas J., Kuter K., Kolasiewicz W., Glowacka U., Ossowska K.

Acta Neurobiologiae Experimentalis

2013

tom 73

nr 1

Motor disturbances in Parkinson’s disease (PD) results from the massive degeneration of dopaminergic neurons and terminals of the nigrostriatal pathway and a decrease in the dopamine (DA) level in the caudate nucleus and putamen. The clinical phase of PD is preceded by a preclinical period where depression is a frequent comorbid disturbance.Dysfunctions of monoaminergic systems could underlie depression in PD. Clinical trials suggest that a treatment with tricyclic antidepressant drugs can be effective in ameliorating depression in PD. Moreover, recent studies have suggested that the administration of pramipexole (the mixed dopamine D2/D3 receptor agonist) may reduce not only motor symptoms (akinesia, rigidity and tremor at rest) but also depression in PD. The aim of the study was to examine the influence of classic tricyclic antidepressant -imipramine and pramipexole on the ‘depressivelike’ behaviour of rats with moderate lesion of the nigrostriatal system. Male Wistar rats were injected bilaterally with 6-OHDA (3.75–15 µg/2.5 µl) into the ventral striatum (vSTR). Imipramine was injected i.p. at a dose of 10 mg/kg once a day and pramipexole s.c. at a dose of 1 mg/kg twice a day for 14 days. The locomotor activity in actometers and behaviour of rats in the forced swimming test (FS) were measured on the 15th day after the surgery. The lesion extent was analysed by HPLC and immunohistochemically. The lesion increased immobility and swimming and decreased climbing in FS, however, it did not influence the locomotor activity of rats. All the lesion-induced disturbances observed in FS were decreased by pramipexole. Imipramine increased only climbing, but had no influence on immobility in lesioned rats. Moreover, imipramine but not pramipexole reduced the locomotor activity in lesioned animals. After the administration of 6-OHDA levels of DA decreased (ca. 45%) in the dorsal striatum (dSTR), vSTR and frontal cortex (FCX). Pramipexole and imipramine injections had no influence on DA levels in lesioned rats. Levels of DA metabolites (DOPAC, HVA) were markedly increased in dSTR and vSTR after injections of pramipexole. Moreover, pramipexole significantly increased the turnover of DOPAC/DA and HVA/DA in dSTR and vSTR in sham-operated and lesioned rats. These results indicate that a relatively moderate dopaminergic lesion which does not produce any motor disturbances, may induce “depressive-like” symptoms which are reversed by dopamine agonist but not by a classic antidepressant. Acknowledgments Study supported by the Project “Depression-Mechanisms-Therapy” (POIG.01.01.02-12-004/09-00), co-financed by EU from the European Regional Development Fund as a part of the Operational Programme “Innovative Economy 2007-2013”

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

80%

Smialowska M., Szewczyk B., Wawrzak-Wlecial A., Domin H.

Acta Neurobiologiae Experimentalis

2013

tom 73

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

Ograniczanie wyników

2 Acta Neurobiologiae Experimentalis

1 Journal of Elementology

1 Berghauzen K.

1 Domin H.

1 Glowacka U.

1 Kolasiewicz W.

1 Kuter K.

1 Nowak G.

1 Ossowska K.

1 Poleszak E.

1 Smialowska M.

1 Szewczyk B.

1 Wardas J.

1 Wawrzak-Wlecial A.

2 2013

1 2006

Wyniki wyszukiwania

Magnesium in pathophysiology and therapy of affective disorders

The influence of imipramine and pramipexole on depressivelike behaviour in an animal model of a pre-clinical stage of Parkinson’s disease

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