| 1. |
- Bontioti, Eleana, et al.
(författare)
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Mechanisms underlying the end-to-side nerve regeneration
- 2009
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Ingår i: International Review of Neurobiology. - 0074-7742. ; 87, s. 251-268
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Forskningsöversikt (refereegranskat)abstract
- End-to-side (ETS) nerve repair is used in selected clinical cases. The mechanisms, by which regeneration into the attached nerve segment is initiated and occur, are still not fully understood. Based on numerous experimental studies, different mechanisms have been Suggested by which regenerating axons are recruited, such as contamination From the proximal nerve segment, collateral sprouting, and terminal regenerating sprouting from the donor nerve. A variety of experimental models, most commonly in the lower and upper extremity of rats, and techniques have been used to shed light on the mechanisms. Retrograde labeling techniques have revealed that collateral sprouting do occur, but is probably, at least as observed in long-term experiments, less important over time. Pruning of branching nerve fibers, induced by the collateral sprouting, is an additional mechanism in this context. Experiments have also focused on the stimuli, including the question of epineurial or perineurial windows, that trigger the sprouting of axons form the donor nerve, which can detected by the use of markers of cellular injury. In die present article, we review studies contributing to clarifications of mechanisms of end-to-side nerve repair, including used experimental techniques. We also stress the importance of the plastic brain.
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| 2. |
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| 3. |
- Fredholm, BB, et al.
(författare)
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Adenosine and brain function
- 2005
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Ingår i: International review of neurobiology. - 0074-7742. ; 63, s. 191-270
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Tidskriftsartikel (refereegranskat)
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| 4. |
- Kiyatkin, Eugene A., et al.
(författare)
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Acute Methamphetamine Intoxication : Brain Hyperthermia, Blood–Brain Barrier, Brain Edema, and morphological cell abnormalities
- 2009
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 88, s. 65-100
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Forskningsöversikt (refereegranskat)abstract
- Methamphetamine (METH) is a powerful and often abused stimulant with potent addictive and neurotoxic properties. While it is generally assumed that multiple chemical substances released in the brain following METH-induced metabolic activation (or oxidative stress) are primary factors underlying damage of neural cells, in this work we present data suggesting a role of brain hyperthermia and associated leakage of the blood-brain barrier (BBB) in acute METH-induced toxicity. First, we show that METH induces a dose-dependent brain and body hyperthermia, which is strongly potentiated by associated physiological activation and in warm environments that prevent proper heat dissipation to the external environment. Second, we demonstrate that acute METH intoxication induces robust, widespread but structure-specific leakage of the BBB, acute glial activation, and increased water content (edema), which are related to drug-induced brain hyperthermia. Third, we document widespread morphological abnormalities of brain cells, including neurons, glia, epithelial, and endothelial cells developing rapidly during acute METH intoxication. These structural abnormalities are tightly related to the extent of brain hyperthermia, leakage of the BBB, and brain edema. While it is unclear whether these rapidly developed morphological abnormalities are reversible, this study demonstrates that METH induces multiple functional and structural perturbations in the brain, determining its acute toxicity and possibly contributing to neurotoxicity.
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| 5. |
- Landgraf, M., et al.
(författare)
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Development and Structure of Motoneurons
- 2006
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 75, s. 33-53
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Forskningsöversikt (refereegranskat)
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| 6. |
- Nyberg, Fred, 1945-
(författare)
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The role of the somatotrophic axis in neuroprotection and neuroregeneration of the addictive brain
- 2009
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 88, s. 399-427
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Forskningsöversikt (refereegranskat)abstract
- Early studies have shown that the abuse of alcohol, central stimulants, and opiates such as heroin destroys brain cells, reducing attention span and memory. However, new research has suggested that there may be a way to regain some of the lost attention and recall. It has recently been shown that brain cells targeted for early death by continued opiate use can be salvaged by injections of synthetic human growth hormone (GH). GH is a polypeptide hormone, normally secreted by the anterior pituitary gland, which stimulates cell growth and controls body metabolism. Recombinant human GH is currently used in replacement therapy to alleviate the symptoms of adults and children with GH deficiency syndrome. The recent observation that GH can reverse morphine-induced cell damage could open the door to new ways of treating and preventing damage from the abuse of opiates in addicts and also of treating cell damage induced by alcohol and central stimulants. This article reviews current knowledge of the somatotrophic axis, including GH and insulin-like growth factor-1 (IGF-1), in the brain and also discusses the potential use of GH/IGF-1 as agents for treatment of brain pathology in addictive diseases.
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| 7. |
- Pekny, Milos, 1965, et al.
(författare)
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The role of astrocytes and complement system in neural plasticity.
- 2007
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Ingår i: International review of neurobiology. - 0074-7742. ; 82, s. 95-111
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Forskningsöversikt (refereegranskat)abstract
- In neurotrauma, brain ischemia or neurodegenerative diseases, astrocytes become reactive (which is known as reactive gliosis) and this is accompanied by an altered expression of many genes. Two cellular hallmarks of reactive gliosis are hypertrophy of astrocyte processes and the upregulation of the part of the cytoskeleton known as intermediate filaments, which are composed of nestin, vimentin, and GFAP. Our aim has been to better understand the function of reactive astrocytes in CNS diseases. Using mice deficient for astrocyte intermediate filaments (GFAP(-/-)Vim(-/-)), we were able to attenuate reactive gliosis and slow down the healing process after neurotrauma. We demonstrated the key role of reactive astrocytes in neurotrauma-at an early stage after neurotrauma, reactive astrocytes have a neuroprotective effect; at a later stage, they facilitate the formation of posttraumatic glial scars and inhibit CNS regeneration, specifically, they seem to compromise neural graft survival and integration, reduce the extent of synaptic regeneration, inhibit neurogenesis in the old age, and inhibit regeneration of severed CNS axons. We propose that reactive astrocytes are the future target for the therapeutic strategies promoting regeneration and plasticity in the brain and spinal cord in various disease conditions. Through its involvement in inflammation, opsonization, and cytolysis, complement protects against infectious agents. Although most of the complement proteins are synthesized in CNS, the role of the complement system in the normal or ischemic CNS remains unclear. Complement activiation in the CNS has been generally considered as contributing to tissue damage. However, growing body of evidence suggests that complement may be a physiological neuroprotective mechanism as well as it may participate in maintenance and repair of the adult brain.
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| 8. |
- Sharma, Hari Shanker, et al.
(författare)
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Cocaine-Induced Breakdown of the Blood–Brain Barrier and Neurotoxicity
- 2009
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 88, s. 297-334
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Forskningsöversikt (refereegranskat)abstract
- Role of cocaine in influencing blood-brain barrier (BBB) function is still unknown. Available evidences suggest that cocaine administration results in acute hyperthermia and alterations in brain serotonin metabolism. Since hyperthermia is capable to induce the breakdown of the BBB either directly or through altered serotonin metabolism, a possibility exists that cocaine may induce neurotoxicity by causing BBB disruption. This hypothesis is discussed in this review largely based on our own laboratory investigations. Our observations in rats demonstrate that cocaine depending on the dose and routes of administration induces profound hyperthermia, increased plasma and brain serotonin levels leading to BBB breakdown and brain edema formation. Furthermore, cocaine was able to enhance cellular stress as seen by upregulation of heat shock protein (HSP 72 kD) expression and resulted in marked neuronal and glial cell damages at the time of the BBB dysfunction. Taken together, these observations are the first to suggest that cocaine-induced BBB disruption is instrumental in precipitating brain pathology. The possible mechanisms of cocaine-induced BBB breakdown and neurotoxicity are discussed.
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| 9. |
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| 10. |
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| 11. |
- Terenghi, Giorgio, et al.
(författare)
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Chapter 21 : Use of stem cells for improving nerve regeneration
- 2009
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Ingår i: International review of neurobiology. - 0074-7742 .- 2162-5514. ; 87, s. 393-403
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Forskningsöversikt (refereegranskat)abstract
- A clear need exists for new surgical approaches to enhance the recuperation of functions after peripheral nerve injury and repair. At present, advances in the regenerative medicine fields of biomaterials, cellular engineering, and molecular biology are all contributing to the development of a bioengineered nerve implant, which could be used clinically as an alternative to nerve autograft. In this review we examine the recent progress in this field, looking in particular at the applicability of Schwann cells and stem cell transplantation to enhance nerve regeneration.
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