| 11. |
- Ekström, Per A R
(author)
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Insulin stimulates ganglionic protein synthesis and reduces thymidine incorporation in support cells of the in vitro regenerating adult frog sciatic sensory neurons
- 1991
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In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 132:2, s. 183-186
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Journal article (peer-reviewed)abstract
- Insulin was tested for effects on crush injured, in vitro regenerating, adult frog sciatic sensory axons. A wide range of insulin concentrations (0.01-10 μg × ml-1) was found to stimulate incorporation of radioactive leucine into ganglionic protein by 50-80%. without affecting the regeneration distance. Simultaneously insulin inhibited the proliferation of the support cells at the crush region by 30%, as measured by thymidine incorporation. Experiments using compartmentalized culture dishes indicated that the proliferation inhibitory effect could be indirect and mediated by the neuronal cells. The results suggest that insulin influences the metabolism of adult peripheral neuronal cell bodies. The stimulated nerve cells could in turn affect the proliferation of support cells in the nerve trunk.
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| 12. |
- Ekström, Per A R, et al.
(author)
-
Leukemia inhibitory factor null mice : Unhampered in vitro outgrowth of sensory axons but reduced stimulatory potential by nerve segments
- 2000
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In: Neuroscience Letters. - 0304-3940. ; 281:2-3, s. 107-110
-
Journal article (peer-reviewed)abstract
- Leukemia inhibitory factor (LIF) is locally up-regulated after peripheral nerve injury and may be involved in the subsequent regeneration. Here, adult mice with or without LIF gene deletions were used to study the role of LIF in regeneration. The results show that axonal regeneration in vitro from dorsal root ganglia (DRGs) was unaffected by LIF deletion. However, segments from wild type mice promoted DRG axonal outgrowth better than segments from LIF deleted animals when in vivo-injured sciatic nerve segments were co-cultured with DRGs from normal adult mice. Addition of LIF could not restore the deficit. This suggests that LIF is engaged in the local regulation of regeneration but not in the regenerative events occuring at the cell body level. (C) 2000 Elsevier Science Ireland Ltd.
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| 13. |
- Ekström, Per A R, et al.
(author)
-
Nerve regeneration and serum levels of insulin-like growth factor-I in rats with streptozotocin-induced insulin deficiency
- 1989
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In: Brain Research. - : Elsevier BV. - 0006-8993. ; 496:1-2, s. 141-147
-
Journal article (peer-reviewed)abstract
- Peripheral nerve regeneration was studied in female Sprague-Dawley rats with streptozotocin-induced insulin deficiency. Nerve regeneration was provoked by a crush lesion on the sciatic nerve 21 days after the streptozotocin injection. The regeneration was assessed by a pinch test at different time-points after injury. The rate ofregeneration in insulin-deficient animals, 2.5 mm/day, was significantly lower than in control animals, 2.9 mm/day(P < 0.05). There was no difference in the initial delay, i.e. the period before regeneration attains a constant velocity. One group of insulin-deficient rats was treated with insulin during the regeneration period by means of implanted osmotic mini-pumps. This treatment prevented the decrease in regenerationsw. After 6 days the sciatic nerves of insulin-deficient rats had regenerated 12.3 ±0.3 mm (mean ±S.E.M.), while the corresponding value for insulin-treated rats was 15.7 ±0.6 mm (P > 0.01). The streptozotocin-treated rats were found to have a 39% reduction in the serum level of insulin-like 1 growth factor-I (IGF-I)_compared to control rats (0.33 ± 0.22 μg/ml and 0.54 ± ml respectively, (P < 0.001). Insulin treatment 1830 1732 during the regeneration period completely restored the IGF-I level back to normal.
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| 14. |
- Ekström, Per, et al.
(author)
-
Calmodulin‐Binding Proteins Within the Slow Phase of Axonal Transport in the Rabbit Vagus Nerve Per Ekstrom and Martin Kanje
- 1987
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In: Journal of Neurochemistry. - : Wiley. - 0022-3042 .- 1471-4159. ; 49:1, s. 146-151
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Journal article (peer-reviewed)abstract
- Abstract: : Calmodulin‐binding proteins (CBPs) in the rabbit vagus nerve were studied by means of calmodulin‐Sepha‐rose affinity chromatography and polyacrylamide gel electrophoresis. The soluble fraction (105g supernatant) of a nerve homogenate contained four CBPs with molecular weights of 44, 55, 91, and 93 kD, respectively. Slowly transported proteins were recovered in the vagus 3 days after injection of [35S]methionine into the nodose ganglion. Four labelled CBPs with molecular weights of 44, 55, 69, and 83 kD, respectively were found. The nodose ganglion con tained two labelled CBPs, 44 and 55 kD. The 55‐kD CBP was identified as tubulin after immunoblotting. In separate experiments it was also shown that bovine brain tubulin bound to the calmodulin column.
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| 15. |
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| 16. |
- EKSTRÖM, Per, et al.
(author)
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Effects of phenothiazines and dibenzazepines on axonal transport and microtubule assembly in vitro
- 1982
-
In: Acta Physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 116:2, s. 121-125
-
Journal article (peer-reviewed)abstract
- Various phenothiazines (thioridazine, trifluoperazine and chlorpromazine) and dibenzazepines (lofepramine, amitriptyline and desipramine) were studied for effects on fast axonal transport (AXT) in vitro in frog sciatic nerves. AXT, measured as the accumulation of (3H) leucine‐labelled proteins in front of a ligature, was inhibited by more then 50% by all the drugs tested at 0.2 mM concentrations. Thioridazine and lofepramine were the most potent inhibitors. These effects were not due to decreased ganglionic incorporation. Some of the drugs also reduced the levels of high energy phosphates, adenosinetriphosphate (ATP) and creatinephosphate (CrP), but not to an extent which is likely to explain the arrested AXT. The polymerization of purified brain tubulin was inhibited by the phenothiazines but unaffected by the dibenzazepines at concentrations which inhibited AXT. Phenothiazines and dibenzazepines are chemically related and known to have a high affinity for calmodulin. The possibility that these drugs interefere with calmodulin regulated processes of importance for AXT will be discussed.
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| 17. |
- Ekström, Per, et al.
(author)
-
Effects of protein kinase inhibitors on regeneration in vitro of adult frog sciatic sensory axons
- 1992
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In: Journal of Neuroscience Research. - : Wiley. - 0360-4012 .- 1097-4547. ; 31:3, s. 462-469
-
Journal article (peer-reviewed)abstract
- The effects of protein kinase inhibitors on regeneration in vitro of adult frog sciatic sensory axons were tested. Regeneration of crush‐injured nerves for 8 days in serum‐free medium was inhibited by staurosporine (100 nM) and H‐7 (100 μM), which are both known to inhibit protein kinase C. With the use of a compartmented culture system it could be shown that H‐7 exerted both local (outgrowth region) and central (ganglia) effects, the latter being more pronounced. The local effects could be due to reduction of Schwann cell proliferation by H‐7. Immunohisto‐chemistry demonstrated the presence of protein kinase C in neuronal cell bodies but not in axonal processes. Proliferation of Schwann cells was accompanied by increased protein kinase C immunoreactivity at the site of injury. H‐7 caused a selective inhibition in the incorporation of radioactive phosphate into one 74 kDa protein of both ganglia and nerve but also a more general decrease in protein labelling. The results show that protein phosphorylations, possibly mediated by protein kinase C, are involved in regeneration‐related mechanisms operating at both local and central levels in the adult frog sciatic sensory axons.
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| 18. |
- Ekström, Per
(author)
-
Increased cyclic AMP in in vitro regenerating frog sciatic nerves inhibits Schwann cell proliferation bur has no effect on axonal outgrowth
- 1995
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In: Journal of Neuroscience Research. - : Wiley. - 0360-4012. ; 42:1, s. 54-62
-
Journal article (peer-reviewed)abstract
- In the present study the role of cAMP for axonal outgrowth and Schwann cell proliferation was studying using the cultured frog sciatic nerve. An intrinsic rise in nerve injury, both in vitro and in vivo. Treatment with 0.1‐1.0μM forskolin, an activator of the cAMP‐generating enzyme adenylyl cyclase, increased the cAMP content up to 13‐fold, but was yet without effect on axonal outgrowth during an 8‐day culturing period. HA‐1004, an inhibitor of cAMP‐dependent protein kinase, also lacked effect on the regeneraton. In contrast, the proliferation of Schwann cells, measured as [3H]thymidine incorporation, was inhibited to about 70% of control by forskolin, whereas HA‐1004 stimulated proliferation to approximately 130% of control. The results suggest that cAMP is involved in the injury‐induced proliferation of Schwann cells of an adult peripheral nerve but that it lacks a central role in the regeneration of sensory axons of such nerves. © 1995 Wiley‐Liss, Inc.
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| 19. |
- Ekström, Per, et al.
(author)
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Inhibition of Fast Axonal Transport by erythro‐9‐[3‐(2‐Hydroxynonyl)]Adenine
- 1984
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In: Journal of Neurochemistry. - : Wiley. - 0022-3042 .- 1471-4159. ; 43:5, s. 1342-1345
-
Journal article (peer-reviewed)abstract
- Abstract: erythro‐9‐[3‐(2‐Hydroxynonyl)]adenine, an inhibitor of protein carboxylmethylation and dynein‐ATPase activity, inhibited fast axonal transport in vitro in frog sciatic nerves. Its site of action might be associated with an ATPase on which transport depends, since specific carboxylmethylation inhibitors lacked effects on transport. The levels of high energy phosphates and protein synthesis were unaffected by the drug at a transport‐inhibiting concentration, making disturbances due to metabolic effects less likely. An erythro‐9‐[3‐(2‐hy‐droxynonyl)]adenine‐sensitive ATPase was looked for in various nerve fractions but has so far not been resolved.
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| 20. |
- Ekström, Per, et al.
(author)
-
The effects of trifluoperazine on fast and slow axonal transport in the rabbit vagus nerve
- 1987
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In: Journal of Neurobiology. - : Wiley. - 0022-3034. ; 18:3, s. 283-293
-
Journal article (peer-reviewed)abstract
- The effects of trifluoperazine (TFP) on fast and slow axonal transport (AXT) of labeled proteins were examined in the rabbit vagus nerve. Cuffs soaked in a 10 mM, but not 0.1 mM or 1 mM, concentration of TFP applied locally around the vagus nerve in vivo blocked both fast and slow AXT, as measured by the accumulation of 3H‐labeled proteins. In vitro, fast AXT was affected by 0.1 mM TFP. The TFP cuff treatment caused a reduction in the number of axonal microtubules (MT) whereas cuffs soaked in saline had no effect. The levels of ATP, ADP, and AMP were not significantly lowered by the TFP treatment. The results suggest that both fast and slow AXT are sensitive to TFP treatment, and that the axonal MT‐system may be the main target of the drug.
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