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Zwierzęta transgeniczne i ich zastosowanie w badaniu choroby Parkinsona

100%
Kosmowska B.
Wszechświat
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2016
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tom 117
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nr 04-06
2

Pramipexole at a low dose induces beneficial effects in the harmaline-induced model of essential tremor in rats

68%
Kosmowska B., Wardas J., Glowacka U., Ananthan S.
Acta Neurobiologiae Experimentalis
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2015
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tom 75
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nr Supl.
BACKGROUND AND AIMS: Harmaline-induced tremor is a model of essential tremor (ET). Tremor induced by harmaline has been suggested to result from activation of the olivo-cerebellar projection. Recent studies have indicated that cerebellum functions may be modulated by dopamine. METHODS: We examined the effects of preferential agonists of dopamine D3 receptors: pramipexole and 7-OH-DPAT on the harmaline-induced tremor in rats. In order to study receptor mechanisms of these drugs rats were pretreated with dopamine D3 receptor antagonists [SB-277011-A (10 mg/kg ip) and SR-21502 (15 mg/ kg ip)], an antagonist of presynaptic D2/D3 receptors [amisulpride (1 mg/kg ip)], or a non-selective antagonist of postsynaptic dopamine receptors [haloperidol (0.5 mg/kg ip)]. RESULTS: The tremor was measured using fully automated Force Plate Actimeters. The following parameters were calculated: power within 0–8 Hz band (AP1) and 9–15 Hz band (AP2), and tremor index (a difference in power between AP2 and AP1). Harmalinetriggered (15 mg/kg ip) tremor was manifested by an increase in AP2 and tremor index. Pramipexole at a low (0.1 mg/kg sc), but not higher doses (0.3 and 1 mg/kg sc) lowered the harmaline-increased AP2. 7-OH-DPAT (0.1 mg/kg sc) reduced AP2 in the harmalinetreated rats. None of the examined dopamine antagonists influenced the above effect of dopamine agonists. In contrast, SB-277011-A administered alone lowered the harmaline-increased AP2. CONCLUSIONS: The present study indicates that pramipexole reduces the harmaline-induced tremor. However, mechanisms underlying its action are still unclear and require further examination. Financial support: Statutory Funds of the Department of NeuroPsychopharmacology, Institute of Pharmacology, PAS; National Science Center (grant OPUS 6, 2013/11/B/NZ4/04565); Southern Research Institute, Birmingham, AL, USA (S. Ananthan) - SR21502 donation. Barbara Kosmowska is a holder of scholarship from the KNOW sponsored by Ministry of Science and Higher Education, Poland.
3
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Latent vaginal trichomonadodid in women as diagnostic-therapeutic problem

59%
Kosmider M., Pilawski Z., Lazar W., Uzar A., Kosmowska B.
Wiadomości Parazytologiczne
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1983
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tom 29
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nr 1-2
4

Brain energy metabolism in neurodegeneration of dopaminergic neurons in animal model of early Parkinson's disease: role of astrocytes

51%
Kuter K., Olech L., Glowacka U., Paleczna M., Kosmowska B., Jurga A.
Acta Neurobiologiae Experimentalis
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2019
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tom 79
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nr Suppl.1
Glial pathology and energy metabolism changes in the brain precede symptoms of Parkinson’s disease (PD) and multiple other neurodegenerative diseases. Astrocytes govern and regulate a large part of the energy metabolism in the brain. Prolonged impairment of astrocytic functions could increase the vulnerability of dopaminergic neurons in the substantia nigra (SN). In this model, 40‑50% of dopaminergic neurons were selectively killed, causing transient locomotor disability compensated with time. We also induced death of astrocytes in the SN, simultaneously activating microglia but sparing the dopaminergic neurons. The astrocytes replenished after toxin withdrawal. We studied multiple markers of energy metabolism and mitochondrial oxidative phosphorylation (OxPhos) complex and supercomplex functioning during the early stages of neurodegeneration and compensation in the SN and striatum (STR). Death of astrocytes diminished the capability of the dopaminergic system to compensate for the degeneration of neurons. It caused a local energy deprivation, a shift in the usage of energy substrates, via increased glycogenolysis and glycolysis markers, ketone bodies availability, and fatty acid transport in remaining glial cells. Increased neuronal expression of CPT1c and astrocytic expression of CPT1a suggest adaptation in fatty acid use. On the other hand, lesion of dopaminergic neurons influenced OxPhos system and enhanced its functioning. Microglia activation also plays an important role in the processes of degeneration, compensation, and energy metabolism regulation. Modulation of its activation phenotypes might be beneficial towards the indicated processes. Astrocyte and microglia energetic influence is one of the factors in the neuronal compensatory mechanisms of dopaminergic system and might have a leading role in presymptomatic PD stages.
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