| 1. |
- Edström, Anders, et al.
(författare)
-
Moderate elevation of extracellular potassium transiently inhibits regeneration of sensory axons in cultured adult sciatic nerves
- 1995
-
Ingår i: Brain Research. - 0006-8993. ; 693:1-2, s. 148-154
-
Tidskriftsartikel (refereegranskat)abstract
- The adult frog dorsal root ganglia (DRG) together with the sciatic nerve (ScN) has previously been shown to survive in organ culture for several days. If a local test crush is made at the beginning of culturing, there is an initial delay of about 3 days before the sensory axons start to grow into the distal nerve stump at a rate of about 0.6-0.9 mm/day. The present results showed that axonal growth was unaffected in preparations maintained for 8 days in medium containing 10 mM K+ (5 mM is the physiological level). In contrast, the outgrowth was markedly reduced by 15 mM K+ and still more by 20 and 25 mM K+. The growth inhibition was partially counteracted by nifedipine, a Ca2+-channel antagonist. Other experiments clearly showed that high K+ exerted its effects during the early phase of the regeneration and lacked effects at later stages. The possibility that Ca2+-binding proteins, e.g., calbindin, which showed immunohistochemical reactivity in different structures, contribute to the growth adaptation to high K+ will be considered. The generality of the findings was supported by inhibition of axonal outgrowth of adult mouse sciatic sensory axons by high K+.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
- Remgård, Pär, et al.
(författare)
-
Calmodulin and In Vitro Regenerating Frog Sciatic Nerves : Release and Extracellular Effects
- 1995
-
Ingår i: European Journal of Neuroscience. - : Wiley. - 0953-816X .- 1460-9568. ; 7:6, s. 1386-1392
-
Tidskriftsartikel (refereegranskat)abstract
- Although calmodulin (CaM) is commonly considered to be an intracellular protein, it has been suggested lately that it is released and exerts functions extracellularly. In the present investigation this was studied in in vitro regenerating adult frog (Rana temporaria) sciatic nerves. Using a multi‐compartment incubation chamber, the non‐neuronal cells in the outgrowth region of such nerves were radiolabelled with amino acid precursors. Based on immunological criteria, these cells were shown to release CaM. When the nerves were treated with CaM, both the outgrowth of sensory axons and the injury‐induced proliferation of non‐neuronal cells were partially inhibited. The inhibitory effects occurred even when the incubation medium contained as little as 30 pM CaM. Furthermore, treatment with anti‐CaM antibodies resulted in reduced outgrowth, which suggested that during normal conditions extracellular CaM is kept at an optimal concentration. Finally, conditioned medium was found to contain several CaM‐binding proteins. The present findings may reflect an earlier unknown function of extracellular CaM in controlling various growth mechanisms in integrated tissues.
|
|
| 5. |
|
|
| 6. |
- Wiklund, Peter, et al.
(författare)
-
Protein kinase C and mouse sciatic nerve regeneration
- 1996
-
Ingår i: Brain Research. - : Elsevier BV. - 0006-8993. ; 715:1-2, s. 145-154
-
Tidskriftsartikel (refereegranskat)abstract
- We have studied the role of protein kinase C (PKC) in peripheral nerve regeneration by using the cultured adult mouse sciatic nerve, which displays regrowth of sensory axons under serum-free conditions. By the use of immunohistochemistry we show that one of the isoforms of PKC, PKCβ, is present in the nerve cell bodies of normal nerves and is upregulated after injury. In spite of this, the specific PKC inhibitor chelerythrine at 5 μM, a concentration well above its IC50 value for PKC, failed to reduce the outgrowth distance of new axons. This was not due to impermeability of the drug, since the same concentration caused a clear reduction of the injury-induced proliferation of Schwann cells in the crush region. Likewise, HA-1004, an inhibitor of cyclic nucleotide-dependent protein kinases, also lacked effect on outgrowth when used on its own, even at very high concentrations (100 μM). In contrast, outgrowth was significantly reduced when 5 μM chelerythrine and 5 μM HA-1004 were used in combination. In conclusion, the present results suggest that PKC-activity is important but not indispensable for the regeneration process. Successful completion of the latter could be achieved by several, perhaps redundant, phosphorylation systems.
|
|
| 7. |
- Wiklund, Peter, et al.
(författare)
-
Protein kinase C inhibition has only a transient growth arresting effect on in vitro regenerating mouse sensory neurons
- 1999
-
Ingår i: Neuroscience Letters. - 0304-3940. ; 275:3, s. 155-158
-
Tidskriftsartikel (refereegranskat)abstract
- Adult mice sensory ganglia were cultured in an extracellular matrix gel. Analyses of extending axons were made 48 h (long-term) or immediately (short-term) after addition of protein kinase inhibitors. Long- and short-term growth was insensitive to protein kinase A/G inhibition by HA-1004. Long-term protein kinase C inhibition by chelerythrine affected only certain, long axons. In the short-term virtually all axon growth was arrested, but largely recovered on the following day. When combined, the drugs inhibited all long- and short-term growth and largely prevented the recovery of the latter. The transient effect by chelerythrine, and the permanent inhibition after combination with HA-1004, suggests compensatory mechanisms, perhaps via other kinases. Copyright (C) 1999 Elsevier Science Ireland Ltd.
|
|
| 8. |
- Wiklund, Peter
(författare)
-
Regeneration of Peripheral Nerves. The role of protein kinases, with emphasis on neurotrophic factor stimulation
- 1999
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The purpose of this study was to investigate the role of protein kinases in peripheral nerve regeneration, with the use of dorsal root ganglia (DRG) and nodose ganglia explants from adult mice. The effects of neurotrophic factor stimulation and protein kinase inhibition were studied for long (days) and short term (minutes) effects. The protein kinase systems studied were protein kinase C (PKC), the cyclic nucleotide dependent protein kinases A and G (PKA, PKG) and the mitogen activated protein kinase (MAPK). When unstimulated regeneration was concerned, inhibition of either PKC or PKA and PKG showed minor or transient effects on both long- and short term axonal outgrowth. Simultaneous inhibition of PKC and PKA/PKG on both unstimulated and NGF stimulated DRG had much stronger effects, suggesting that complementary kinase systems work together during outgrowth. Inhibition of MAPK also lacked effects on unstimulated DRG or nodose ganglia. When neurotrophic factors were used on DRG, MAPK inhibition effectively inhibited both NGF and glial cell line-derived (GDNF) stimulated outgrowth. In contrast to this, neurotrophin-3 (NT-3) stimulated DRG outgrowth was further increased after inhibition of MAPK. Neurotrophin-4 (NT-4) activated MAPK and strongly stimulated axonal outgrowth from the nodose ganglion; yet MAPK inhibition was without effect on the NT-4 stimulated nodose outgrowth. The results thus show that the relative importance of MAPK varies between unstimulated and different types of stimulated growth in peripheral neurons, perhaps in a neuronal population specific way.
|
|
| 9. |
- Xu, Youshi, et al.
(författare)
-
On the utilization of voice-unused resource for data transmission in PRMA systems
- 1998
-
Ingår i: IEEE 1998 International Conference on Universal Personal Communications, Florence, It., Oct 05-09, 1998. ICUPC '98. Vol. 2. - : IEEE. ; , s. 1043-1047
-
Konferensbidrag (refereegranskat)abstract
- In the paper voice-unused resource in a voice-only PRMA system is analyzed. A mechanism for the detection of voice-unused resource is proposed. How to use the voice-unused resource for data transmission is proposed. Therefore, the voice subsystem is totally a voice-only PRMA system, and the existence of data transmission just improves the channel utilization efficiency, without any influence on the performance of voice communications. Simulation results show that a significant amount of data traffic can be supported by the voice-unused resource.
|
|
