Showing papers by "Jenny Karlsson published in 1998"
TL;DR: Findings suggest that cell death occurring during nigral transplantation is not primarily due to excitotoxicity.
Abstract: Two groups of hemiparkinsonian rats received grafts of embryonic ventral mesencephalon with or without the addition of the NMDA receptor antagonist (+)dizocilpine hydrogen maleate (MK-801). When added to the cell suspension, a 10 microM concentration of MK-801 did not enhance the survival of tyrosine hydroxylase positive neurones in the grafts. These findings suggest that cell death occurring during nigral transplantation is not primarily due to excitotoxicity.
22 citations
TL;DR: It is found that PBN does not increase the survival of cultured embryonic dopaminergic neurons subjected to serum deprivation, whereas the antioxidant and lipid peroxidation inhibitor lazaroid U-83836E does and adult nigral neuron subjected to a progressive retrograde 6-OHDA lesion are not protected by systemic treatment with PBN.
21 citations
TL;DR: Linomide pre-treatment profoundly reduced the injury-induced apoptotic death of neurons and satellite cells in both systems, suggesting that modulation of the inflammatory cytokine cascade is a promising road to nerve cell rescue.
Abstract: Neuronal death after injury or disease could result from imbalanced cytokine expression. Linomide (LS-2616, quinoline-3-carboxamide), a synthetic immunomodulator with effects on cytokine production, suppresses autoimmune diseases of the nervous system. Here adult mice were pre-treated with 200 mg/kg/day of Linomide for 9 days, after which the sciatic nerves were crushed. After another 10 days of Linomide treatment the dorsal root ganglia were dissected out and stained for apoptosis, either immediately or after 2 days in culture, which increases cell death. Superior cervical ganglia were also cultured for 2 days. The Linomide pretreatment profoundly reduced (approximately 60-80%) the injury-induced apoptotic death of neurons and satellite cells in both systems. The results suggest that modulation of the inflammatory cytokine cascade is a promising road to nerve cell rescue.
13 citations
01 Jan 1998
TL;DR: It is found that PBN does not increase the survival of cultured embryonic dopaminergic neurons subjected to serum deprivation, whereas the antioxidant and lipid peroxidation inhibitor lazaroid U-83836E does, and adult nigral neuron subjected to a progressive retrograde 6-OHDA lesion are not protected by systemic treatment with PBN.
Abstract: Reactive oxygen species are thought to be involved in the death of dopaminergic neurons in Parkinson's disease as well as in . transplanted embryonic dopaminergic neurons. The spin-trap agent a-phenyl-N-tert-butyl nitrone PBN reacts directly with radical species and may thereby prevent them from damaging important cellular molecules such as membrane lipids. We found that PBN does not increase the survival of cultured embryonic dopaminergic neurons subjected to serum deprivation, whereas the antioxidant and lipid peroxidation inhibitor lazaroid U-83836E does. Moreover, PBN does not increase the survival of grafted embryonic dopaminergic . neurons or graft efficacy monitored as changes in drug-induced motor asymmetry in hemiparkinsonian rats when the spin-trap agent is given intraperitoneally to the graft recipient or is added to the solutions used when preparing tissue for transplantation. Another spin-trap . . agent, a- 4-pyridyl-1-oxide -N-tert-butyl nitrone POBN also failed to protect neurons when given to graft recipients in the same experimental paradigm. Finally, we found that adult nigral neurons subjected to a progressive retrograde 6-OHDA lesion are not protected by systemic treatment with PBN. Even though reduction of oxidative stress by overexpression of superoxide dismutase or addition of lazaroids have previously been shown to enhance the survival of cultured and grafted dopaminergic neurons, spin-trap agents PBN and POBN do not provide protection in these experimental paradigms. This may be due to antioxidants and spin-trap agents interfering in different steps of free radical-induced cell damage. q 1998 Elsevier Science B.V. All rights reserved.
2 citations