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| 2. |
- Bergström, Martin, et al.
(författare)
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Sense of coherence: definition and explanation
- 2006
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Ingår i: International Journal of Social Welfare. - : Wiley. - 1369-6866 .- 1468-2397. ; 15:3, s. 219-229
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Tidskriftsartikel (refereegranskat)abstract
- The present study is one of a few that have used "sense of coherence" (SOC) as a dependent variable in an explanatory model. After studying three different samples - 680 students, 180 parents and 315 couples - we conclude that family relational and psychopathological variables contribute significantly to the explanation of SOC (explained variance between 10-27 and 26-50 per cent). In total, we obtained an explained variance of between 42 and 64 per cent. This leads us to the conclusion that in all three samples, SOC is multifaceted and thereby is more than simply an opposite state to depression. Context may play an important part in the explanation of SOC.
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| 3. |
- Carlsson, Thomas, et al.
(författare)
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Graft placement and uneven pattern of reinnervation in the striatum is important for development of graft-induced dyskinesia.
- 2006
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Ingår i: Neurobiology of Disease. - : Elsevier BV. - 0969-9961. ; 21:3, s. 657-668
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Tidskriftsartikel (refereegranskat)abstract
- In two recent double-blind clinical trials of fetal ventral mesencephalic cell transplants into the striatum in patients with Parkinson's disease (PD), a significant proportion of the grafted patients developed dyskinetic side effects, which were not seen in the sham operated patients. Comparison between dyskinetic and non-dyskinetic grafted patients in one of the trials suggested that an uneven pattern of striatal reinnervation might be the leading cause of the dyskinesias. Here, we studied the importance of graft placement for the development of dyskinesias in parkinsonian rats. Abnormal involuntary movements resembling peak-dose dyskinesias seen in PD patients were induced by daily injections of L-DOPA for 6 weeks. The dyskinetic animals received about 130.000 fetal ventral mesencephalic cells as single grafts placement in the rostral or the caudal aspect of the head of striatum. The results show that grafts placed in the caudal, but not the rostral, part are effective in reducing the L-DOPA-induced limb and orolingual dyskinesia, predominantly seen as hyperkinesia. The same grafts, however, also induced a new type of dyskinetic behavior after activation with amphetamine, which were not seen in non-grafted lesion controls. The severity of these abnormal involuntary movements was significantly correlated with a higher graft-derived dopaminergic reinnervation in the caudal aspect of the head of striatum relative to the rostral part. The results indicate that graft-induced dyskinesias in PD patients may be linked to single, small graft deposits that provide an uneven, patchy reinnervation of the putamen.
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| 4. |
- Carta, Manolo, et al.
(författare)
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Role of striatal l-DOPA in the production of dyskinesia in 6-hydroxydopamine lesioned rats.
- 2006
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Ingår i: Journal of Neurochemistry. - : Wiley. - 1471-4159 .- 0022-3042. ; 96:6, s. 1718-1727
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Tidskriftsartikel (refereegranskat)abstract
- We explored possible differences in the peripheral and central pharmacokinetics of L-DOPA as a basis for individual variation in the liability to dyskinesia. Unilaterally, 6-hydroxydopamine (6-OHDA) lesioned rats were treated chronically with L-DOPA for an induction and monitoring of abnormal involuntary movements (AIMs). Comparisons between dyskinetic and non-dyskinetic cases were then carried out with regard to plasma and striatal L-DOPA concentrations, tissue levels of dopamine (DA), DA metabolites, and serotonin. After a single intraperitoneal injection of L-DOPA, plasma L-DOPA concentrations did not differ between dyskinetic and non-dyskinetic animals, whereas peak levels of L-DOPA in the striatal extracellular fluid were about fivefold larger in the former compared with the latter group. Interestingly, the time course of the AIMs paralleled the surge in striatal L-DOPA levels. Intrastriatal infusion of L-DOPA by reverse dialysis concentration dependently induced AIMs in all 6-OHDA lesioned rats, regardless of a previous priming for dyskinesia. Steady-state levels of DA and its metabolites in striatal and cortical tissue did not differ between dyskinetic and non-dyskinetic animals, indicating that the observed difference in motor response to L-DOPA did not depend on the extent of lesion-induced DA depletion. These results show that an elevation of L-DOPA levels in the striatal extracellular fluid is necessary and sufficient for the occurrence of dyskinesia. Individual differences in the central bioavailability of L-DOPA may provide a clue to the varying susceptibility to dyskinesia in Parkinson's disease.
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| 6. |
- Cenci Nilsson, Angela, et al.
(författare)
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Post- versus presynaptic plasticity in L-DOPA-induced dyskinesia.
- 2006
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Ingår i: Journal of Neurochemistry. - : Wiley. - 1471-4159 .- 0022-3042. ; 99:2, s. 381-392
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Tidskriftsartikel (refereegranskat)abstract
- L-3,4-dihydroxyphenylalanine (L-DOPA) remains the most efficacious drug for the treatment of Parkinson's disease (PD), but causes adverse effects that limit its utility. L-DOPA-induced dyskinesia (abnormal involuntary movements) is a significant clinical problem that attracts growing scientific interest. Current notions attribute the development of dyskinesia to two main factors, viz. the loss of nigrostriatal dopamine (DA) projections and the maladaptive changes produced by L-DOPA at sites postsynaptic to the nigrostriatal neuron. Basic research in the past 15 years has placed a lot of emphasis on the postsynaptic plasticity associated with dyskinesia, but recent experimental work shows that also some presynaptic factors, involving the regulation of L-DOPA/DA release and metabolism in the brain, may show plasticity during treatment. This review summarizes significant studies of L-DOPA-induced dyskinesia in patients and animal models, and outlines directions for future experiments addressing mechanisms of presynaptic plasticity. These investigations may uncover clues to the varying susceptibility to L-DOPA-induced dyskinesia among PD patients, paving the way for tailor-made treatments.
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| 7. |
- Cenci Nilsson, Angela, et al.
(författare)
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Ratings of L-DOPA-induced dyskinesia in the unilateral 6-OHDA lesion model of Parkinson's disease in rats and mice.
- 2007
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Ingår i: Current protocols in neuroscience / editorial board, Jacqueline N. Crawley ... [et al.]. - : Wiley. - 1934-8576. ; Chapter 9:Oct, s. 9-25
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Tidskriftsartikel (refereegranskat)abstract
- This unit provides detailed protocols for establishing rodent models of L-DOPA-induced dyskinesia. The 6-hydroxydopamine (6-OHDA) lesion procedure is described in more detail for mice than for rats since the lesioning procedure in rats has been described extensively in previous work and is less difficult to perform. Unlike primate models, rodent models of L-DOPA-induced dyskinesia are relatively simple and fast to set up, thus being affordable to most laboratories. These models allow for studying the dyskinetic complications of L-DOPA treatment on large groups of animals under strictly controlled experimental conditions. Along with information and structured protocols for the practical execution of the test, this unit provides a detailed description of the rating scale and the phenomenology of rodent abnormal involuntary movements, and suggestions for beginners.
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| 8. |
- Dekundy, Andrzej, et al.
(författare)
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Modulation of l-DOPA-induced abnormal involuntary movements by clinically tested compounds: Further validation of the rat dyskinesia model.
- 2007
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Ingår i: Behavioural Brain Research. - : Elsevier BV. - 0166-4328. ; 179:1, s. 76-89
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Forskningsöversikt (refereegranskat)abstract
- l-DOPA-induced dyskinesia (LID) is a major complication of the pharmacotherapy of Parkinson's Disease. A model of LID has recently been described in rats with unilateral 6-hydroxydopamine (6-OHDA) lesions. In the present study, the model was used in order to compare the efficacies of some clinically available compounds that have shown antidyskinetic effects in nonhuman primate models of LID and/or in patients, namely, amantadine (20 and 40 mg/kg), buspirone (1, 2 and 4 mg/kg), clonidine (0.01, 0.1 and 1 mg/kg), clozapine (4 and 8 mg/kg), fluoxetine (2.5 and 5 mg/kg), propranolol (5, 10 and 20 mg/kg), riluzole (2 and 4 mg/kg), and yohimbine (2 and 10 mg/kg). Rats were treated for 3 weeks with l-DOPA for an induction and monitoring of abnormal involuntary movements (AIMs) prior to the drug screening experiments. The antidyskinetic drugs or their vehicles were administered together with l-DOPA, and their effects were evaluated according to a randomized cross-over design both on the AIM rating scale and on the rotarod test. Most of the compounds under investigation attenuated the l-DOPA-induced axial, limb and orolingual AIM scores. However, the highest doses of many of these substances (but for amantadine and riluzole) had also detrimental motor effects, producing a reduction in rotarod performance and locomotor scores. Since the present results correspond well to existing clinical and experimental data, this study indicates that axial, limb and orolingual AIMs possess predictive validity for the preclinical screening of novel antidyskinetic treatments. Combining tests of general motor performance with AIMs ratings in the same experiment allows for selecting drugs that specifically reduce dyskinesia without diminishing the anti-akinetic effect of l-DOPA.
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