The present study showed that insulin (0.01 pg/ml, = 2 nM) inhibited [3H]-thymidine incorporation in support cells, most likely Schwann cells, of the cultured frog sciatic nerve. A 25-35% inhibition took place in regenerating nerve preparations as well as in preparations devoid of neuronal protein s
Increased cyclic AMP in in vitro regenerating frog sciatic nerves inhibits Schwann cell proliferation bur has no effect on axonal outgrowth
✍ Scribed by P. A. R. Ekström
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 891 KB
- Volume
- 42
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
✦ Synopsis
In the present study the role of cAMP for axonal outgrowth and Schwann cell proliferation was studied using the cultured frog sciatic nerve. An intrinsic rise in nerve and ganglionic cAMP could be measured as a response to nerve injury, both in vitro and in vivo. Treatment with 0.1-1.0 p M 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 regeneration. 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.
📜 SIMILAR VOLUMES