| 1. |
- Povlsen, Bo, et al.
(author)
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Functional evaluation of regenerated and misrouted axons to glabrous and hairy skin of the rat hind foot after sciatic neurotomy and suture
- 1995
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In: Experimental Neurology. - : Elsevier BV. - 0014-4886 .- 1090-2430. ; 132:1, s. 99-104
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Journal article (peer-reviewed)abstract
- The function of misrouted regenerated polymodal nociceptor C-fibers and low-threshold mechanoreceptive axons in the lateral plantar nerve (LPN) and in the foot branch of the superficial peroneal nerve (fSPN) was evaluated 3 months after unilateral sciatic neurotomy and suture. Two weeks before evaluation the tibial fascicle (or the peroneal fascicle) above the neurotomy was cut and tied off. In this way only functional regeneration of misrouted axons was tested in the LPN (or the fSPN). In regenerated animals the glabrous skin area had no functional fSPN-related low-threshold mechanoreceptive axons. However, the hairy fSPN skin area showed function of misrouted LPN-related low-threshold mechanoreceptive axons. In both the glabrous skin domain innervated by the LPN and the hairy skin area supplied by the fSPN, functional regeneration of misrouted polymodal nociceptor C-fibers was found. We conclude that functional regeneration of misrouted axons related to polymodal nociceptive units and low-threshold mechanoreceptive units is more efficient in hairy skin of the rat foot whereas only misrouted polymodal nociceptor C-fibers recover function in glabrous skin.
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| 2. |
- Büki, Andras, 1966-, et al.
(author)
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Moderate Posttraumatic Hypothermia Decreases Early Calpain-Mediated Proteolysis and Concomitant Cytoskeletal Compromise in Traumatic Axonal Injury
- 1999
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In: Experimental Neurology. - : Academic Press. - 0014-4886 .- 1090-2430. ; 159:1, s. 319-328
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Journal article (peer-reviewed)abstract
- Traumatic brain injury (TBI) in animals and man generates widespread axonal injury characterized by focal axolemmal permeability changes, induction of calpain-mediated proteolysis, and neurofilament side-arm modification associated with neurofilament compaction (NFC) evolving to axonal disconnection. Recent observations have suggested that moderate hypothermia is neuroprotective in several models of TBI. Nevertheless, the pathway by which hypothermia prevents traumatic axonal injury (TAI) is still a matter of debate. The present study was conducted to evaluate the effects of moderate, early posttraumatic hypothermia on calpain-mediated spectrin proteolysis (CMSP), implicated in the pathogenesis of TAI. Using moderate (32 degrees C) hypothermia of 90 min duration without rewarming, the density of CMSP immunoreactive/damaged axons was quantified via LM analysis in vulnerable brain stem fiber tracts of hypothermic and normothermic rats subjected to impact acceleration TBI (90 min postinjury survival). To assess the influence of posthypothermic rewarming, a second group of animals was subjected to 90 min of hypothermia followed by 90 min of rewarming to normothermic levels when CMSP was analyzed to detect if any purported CMSP prevention persisted (180 min postinjury survival). Additionally, to determine if this protection translated into comparable cytoskeletal protection in the same foci showing decreased CMSP, antibodies targeting altered/compacted NF subunits were also employed. Moderate hypothermia applied in the acute postinjury period drastically reduced the number of damaged axons displaying CMSP at both time points and significantly reduced NFC immunoreactivity at 180 min postinjury. These results suggest that the neuroprotective effects of hypothermia in TBI are associated with the inhibition of axonal/cytoskeletal damage.
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| 3. |
- Ekegren, Titti, et al.
(author)
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Methionine adenosyltransferase activity in erythrocytes and spinal cord of patients with sporadic amyotrophic lateral sclerosis
- 1999
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In: Experimental Neurology. - 0014-4886 .- 1090-2430. ; 158:2, s. 422-427
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Journal article (peer-reviewed)abstract
- The role of transmethylation mechanisms in the etiology of amyotrophic lateral sclerosis (ALS) is hitherto unexplored. The activity of L-methionine S-adenosyltransferase (MAT), a regulatory enzyme of S-adenosylmethionine biosynthesis, was investigated in erythrocytes of 21 patients with ALS, spinal cord specimens of 7 ALS patients, and matched controls. In ALS patients the activity of MAT in erythrocytes was sex-dependent. In comparison with controls, the male group presented a 33% higher Vmax (PF0.05) and a 41% decrease in the affinity of MAT for methionine (Km, PF0.05). The type of ALS onset (limb or bulbar), age, or duration of the disease did not influence erythrocyte MAT activity. In the spinal cord, the activity of MAT was homogeneously distributed through dorsal horn, ventral horn, and white matter. Comparisons between data from controls and ALS patients and analysis of sex effect showed no significant differences. The kinetic difference of erythrocyte MAT in the male group of ALS patients might be interesting to explore since it is well known that there is a male predominance of 1.5 to 2.5:1 inALS.
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| 4. |
- Liu, Li, et al.
(author)
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Clusterin upregulation following rubrospinal tract lesion in the adult rat
- 1999
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In: Experimental Neurology. - : Elsevier BV. - 0014-4886 .- 1090-2430. ; 157:1, s. 69-76
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Journal article (peer-reviewed)abstract
- We have examined the expression of the multifunctional protein clusterin in the axotomized red nucleus, at the lesion site in the lateral funiculus of C3, as well as along the Wallerian degeneration in the lateral funiculus of T1. There was a marked increase in clusterin-immunoreactivity (IR) and clusterin mRNA in red nucleus nerve cell bodies. An early, transient occurrence of large, heavily clusterin-IR globules were found in axons in the spinal cord at the lesion site in C3 as well as a marked upregulation of mRNA for clusterin, presumably associated with reactive astrocytes and oligodendrocytes from 1 to 4 weeks postoperatively. Clusterin-IR and its mRNA were markedly increased in the zone of Wallerian degeneration at T1, where some strongly expressing cells were identified as oligodendrocytes. Taken together with previous changes in clusterin expression following peripheral nerve and dorsal root injury, we suggest that this protein is involved in regenerative as well as degenerative neural responses.
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| 5. |
- Petersén, Åsa, et al.
(author)
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Recent advances on the pathogenesis of Huntington's disease
- 1999
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In: Experimental Neurology. - : Elsevier BV. - 0014-4886 .- 1090-2430. ; 157:1, s. 1-18
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Journal article (peer-reviewed)abstract
- We review recent advances regarding the pathogenesis of Huntington's disease (HD). This genetic neurodegenerative disorder is caused by an expanded CAG repeat in a gene coding for a protein, with unknown function, called huntingtin. There is selective death of striatal and cortical neurons. Both in patients and a transgenic mouse model of the disease, neuronal intranuclear inclusions, immunoreactive for huntingtin and ubiquitin, develop. Huntingtin interacts with the proteins GAPDH, HAP-1, HIP1, HIP2, and calmodulin, and a mutant huntingtin is specifically cleaved by the proapoptotic enzyme caspase 3. The pathogenetic mechanism is not known, but it is presumed that there is a toxic gain of function of the mutant huntingtin. Circumstantial evidence suggests that excitotoxicity, oxidative stress, impaired energy metabolism, and apoptosis play a role.
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| 6. |
- von Euler, Mia, 1967-, et al.
(author)
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Clip compression injury in the spinal cord : a correlative study of neurological and morphological alterations
- 1997
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In: Experimental Neurology. - New York, USA : Academic Press. - 0014-4886 .- 1090-2430. ; 145:2 Pt 1, s. 502-510
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Journal article (peer-reviewed)abstract
- Rats subjected to experimental spinal cord compression of different degrees induced by aneurysm clips were neurologically tested 3 and 5 weeks postinjury. The development of spinal cord tissue destruction over time was similar to what has been described for other experimental spinal cord injuries with characteristics such as early edema, axonal swelling, and later necrosis. Three weeks after injury a reactive gliosis was found at the injury epicenter and regenerating axons could be identified in the otherwise necrotic cavity. The extent of degeneration was highly correlated with the closing force of the aneurysm clip. The results of a number of neurological tests were correlated to the degree of clip-induced compression, to lesion volume, and to the remaining area of white matter at the epicenter. The neurological tests with the highest correlation to morphological descriptors were beam walk (r(s) = 0.89-0.95) and motor performance score (r(s) = 0.88-0.92). We conclude that the motor performance score, previously validated for photochemically induced ischemic spinal cord injuries, is equally suitable for clip compression injuries as a fast and reliable neurological test paradigm.
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| 7. |
- von Euler, Mia, 1967-, et al.
(author)
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Motor Performance Score : A New Algorithm for Accurate Behavioral Testing of Spinal Cord Injury in Rats
- 1996
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In: Experimental Neurology. - New York, USA : Academic Press. - 0014-4886 .- 1090-2430. ; 137:2, s. 242-254
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Journal article (peer-reviewed)abstract
- To evaluate the usefulness of standard neurological tests in predicting the neurological outcome after photochemically induced spinal cord lesions in rats, we inflicted injuries of different severity to adult female rats. The behavior of the rats was followed for 6 weeks and the results of the behavioral tests were correlated with morphological indicators of tissue destruction at the end of this period. We found many behavioral tests to be highly correlated with the loss of tissue, whereas some tests were inaccurate in correlating with degree of tissue destruction. Motor score, beam walk, and righting reflex were all highly correlated with the volume of the lesion as well as with the depth of the lesion cavity at its epicenter. We propose a protocol for neurological evaluation of this type of spinal cord injury consisting of six individual tests, hierarchally organized such that injured rats can be divided into 11 groups of neurological deficit, scored from 10 to 0. This so-called motor performance score is fast and easy to perform and shows high correlation with the lesion volume, and is thus suitable for neurological evaluation of photochemically induced spinal cord injury.
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