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- Kokaia, Zaal, et al.
(författare)
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Co-expression of TrkB and TrkC receptors in CNS neurones suggests regulation by multiple neurotrophins
- 1995
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Ingår i: NeuroReport. - : Ovid Technologies (Wolters Kluwer Health). - 1473-558X .- 0959-4965. ; 6:5, s. 769-772
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Tidskriftsartikel (refereegranskat)abstract
- Using double-label in situ hybridization, we have explored the possibility that individual CNS neurones can co-express mRNAs for the high-affinity receptors of brain-derived neurotrophic factor and neurotrophin-3, TrkB and TrkC, respectively. The vast majority of TrkC mRNA-containing neurones in the hippocampal formation and cerebral cortex were also labelled for TrkB mRNA. Cells expressing only TrkB or TrkC mRNA were very scarce in these regions, representing < 15% of all labelled cells. These findings suggest that the same cortical or hippocampal neurone can be regulated by several members of the neurotrophin family, which may be important both during development and in response to physiological activity and pathological conditions.
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| 2. |
- Okonkwo, David O., et al.
(författare)
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Cyclosporin A limits calcium-induced axonal damage following traumatic brain injury
- 1999
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Ingår i: NeuroReport. - : Lippincott Williams & Wilkins. - 0959-4965 .- 1473-558X. ; 10:2, s. 353-358
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Tidskriftsartikel (refereegranskat)abstract
- In traumatic axonal injury, Ca2+ influx across a focally damaged axolemma precipitates local mitochondrial failure, degradation of the subaxolemmal spectrin network and compaction of neurofilaments, which collectively contribute to axonal failure. In previous studies, cyclosporin A pretreatment preserved mitochondrial integrity and attenuated axonal failure following trauma. Here we investigate whether this CsA-linked protection was related to the concomitant blunting of intra-axonal, Ca2+-induced cytoskeletal changes in traumatic axonal injury, assessed with antibodies targeting spectrin proteolysis and neurofilament compaction. CsA pretreatment dramatically reduced Ca2+-induced cytoskeletal damage following injury; CsA-treated rats, compared with vehicle-treated rats, displayed a 70% decrease in immunoreactive/damaged profiles. We suggest that CsA-mediated preservation of mitochondrial integrity enables the restoration of ionic and metabolic homeostasis thereby short-circuiting Ca2+-induced proteolysis in injured axons.
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| 3. |
- Rinken, A, et al.
(författare)
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Serotonergic agonists behave as partial agonists at the dopamine D2 receptor
- 1999
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Ingår i: NeuroReport. - : Ovid Technologies (Wolters Kluwer Health). - 1473-558X .- 0959-4965. ; 10:3, s. 493-495
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Tidskriftsartikel (refereegranskat)abstract
- RAT dopamine D2short receptors expressed in CHO cells were characterized by activation of [35S]GTPgammaS binding. There were no significant differences between the maximal effects seen in activation of [35S]GTPgammaS binding caused by dopaminergic agonists, but the effects of 5-HT, 8OH-DPAT and 5-methoxytryptamine amounted to 47 +/- 7%, 43 +/- 5% and 70 +/- 7% of the dopamine effect, respectively. The dopaminergic antagonist (+)butaclamol inhibited activations of both types of ligands with equal potency (pA2 = 8.9 +/- 0.1), indicating that only one type of receptor is involved. In competition with [3H]raclopride binding, dopaminergic agonists showed 53 +/- 2% of the binding sites in the GTP-dependent high-affinity state, whereas 5-HT showed only 20 +/- 3%. Taken together, the results indicate that serotonergic agonists behave as typical partial agonists for D2 receptors with potential antiparkinsonian activity.
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| 4. |
- Van Landeghem, G F, et al.
(författare)
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Transferrin C2, metal binding and Alzheimer's disease.
- 1998
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Ingår i: NeuroReport. - 0959-4965 .- 1473-558X. ; 9:2, s. 177-9
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Tidskriftsartikel (refereegranskat)abstract
- Significant associations between the transferrin (TF) variant C2 and a number of disorders suspected to be caused by oxygen free radicals have been reported. Thus an increased frequency of the TFC2 variant has been found in patients with Alzheimer's disease (AD), and it has been hypothesized that AD is caused by free radical damage due to defective binding of iron and aluminium by TFC2. In a study of 64 patients with AD from northern Sweden we were able to confirm the association between TFC2 and AD, but there were no significant differences between TFC2 and other TF variants with respect to the binding of iron and aluminium.
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