| 1. |
- Karlsson, Jenny, et al.
(författare)
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Increased survival of embryonic nigral neurons when grafted to hypothermic rats
- 2000
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Ingår i: NeuroReport. - 0959-4965. ; 11:8, s. 1665-1668
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Tidskriftsartikel (refereegranskat)abstract
- Hypothermia can reduce neuronal death caused by ischemia and traumatic brain injury. We therefore investigated whether mild hypothermia in rats receiving a transplant of embryonic mesencephalic rat tissue increases survival of the implanted dopaminergic neurons. Mild hypothermia (32-33°C) during graft implantation and for the following 90 min significantly increased the survival of transplanted dopaminergic neurons to 171% of control values in normothermic (37°C) rats. This demonstrates that treatment of the graft recipient for a relatively short period during and after surgery has a favorable effect on the survival of grafted dopaminergic neurons. These findings may be of importance for clinical neural transplantation trials which are in need of procedures that improve transplant survival. (C) 2000 Lippincott Williams and Wilkins.
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| 2. |
- Khaspekov, Leonid, et al.
(författare)
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Sublethal in vitro glucose-oxygen deprivation protects cultured hippocampal neurons against a subsequent severe insult
- 1998
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Ingår i: NeuroReport. - 0959-4965. ; 9:7, s. 1273-1276
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Tidskriftsartikel (refereegranskat)abstract
- Rat and gerbil hippocampus exposed to a sublethal period of ischemia becomes resistant to a subsequent period of lethal ischemia induced several days later, a phenomenon referred to as ischemic preconditioning. Here we describe ischemic preconditioning induced in vitro in cultured hippocampal neurons. Mixed neuroglial hippocampal cell cultures of 14-17 DIV were exposed to a combined glucose and oxygen deprivation (GOD). Cultures subjected to 90 min, but not 60 min, of GOD showed extensive degeneration after a 1 day recovery period. An episode of 60 min of preconditioning GOD followed 1 and 2 days later by 90 min of GOD resulted in 40-60% protection. The data demonstrate that ischemic preconditioning can be mimicked in an in vitro hippocampal cell culture system.
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| 3. |
- Ren Hu, Bing, et al.
(författare)
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Changes in tyrosine phosphorylation in neocortex following transient cerebral ischaemia
- 1993
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Ingår i: NeuroReport. - 0959-4965. ; 4:2, s. 219-222
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Tidskriftsartikel (refereegranskat)abstract
- Growth factor receptors activate protein tyrosine kinases, which are important for cell growth and survival. The protein tyrosine kinase (PTK) activity and the levels of phosphotyrosine (Ptyr) containing proteins were studied in the rat neocortex exposed to 15 min of transient cerebral ischaemia. The levels of the Ptyr containing proteins increase during recovery in the synaptosomal fraction, while the changes in the light membrane fraction are less marked. Protein tyrosine phosphorylation in the cytosol decreases. The differential changes in the levels of phosphotyrosine proteins in the particulate and cytosolic fractions suggest that the signal cascade from membrane bound receptors through tyrosine phosphorylation in the cytosol may be interrupted following ischaemia. This may be of importance for the development of neuronal damage.
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| 4. |
- Shamloo, Mehrdad, et al.
(författare)
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Rapid decline in protein kinase Cγ levels in the synaptosomal fraction of rat hippocampus after ischemic preconditioning
- 1999
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Ingår i: NeuroReport. - : Ovid Technologies (Wolters Kluwer Health). - 0959-4965. ; 10:5, s. 931-935
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Tidskriftsartikel (refereegranskat)abstract
- Neurons can be preconditioned against ischemic damage by a brief sublethal period of ischemia, applied several days before the second insult. Here we report on changes in the distribution and the levels of protein kinase Cγ (PKCγ) in nonconditioned and preconditioned rat hippocampal CA1 and neocortex regions after a 9 min ischemic episode induced by two-vessel occlusion ischemia. At the end of the second ischemia we found significantly lower levels of PKCγ in the CA1 region but not neocortex of preconditioned brains than in non-conditioned brains. Protein kinase Cγ levels in both CA1 and neocortex decrease simultaneously in the cytosolic fractions. We conclude that PKCγ is translocated to cell membranes during ischemia and is rapidly removed or degraded during the second otherwise lethal ischemic insult in preconditioned brains. The data suggest that ischemic preconditioning enhances downregulation of cell signaling mediated by PKCγ and may thereby provide neuroprotection.
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