Table 1.
A cyclic GMP analog increases AChR aggregation and inhibitors of guanlylate cyclase and cGMP-dependent protein kinase reduce endogenous AChR aggregation at the embryonic neuromuscular junction.
| Experiment No. | Treatment | AChR aggregate area (% ± SEM) | Area ratio experimental: Control | P vs. Control |
|---|---|---|---|---|
| 1 | Control (unskinned) | 0.18 ± 0.07 | -- | -- |
| 8-Br-cGMP (100 μM) | 0.74 ± 0.10 | 4.0 | 0.001 | |
| 2 | Control (skinned) | 0.34 ± 0.06 | -- | -- |
| 8-Br-cGMP (100 μM) | 0.987 ± 0.20 | 2.9 | 0.004 | |
| 3 | Control (unskinned) | 1.36 ± 0.21 | -- | -- |
| ODQ (50 μM) | 0.21 ± 0.06 | 0.15 | 5 × 10−5 | |
| 4 | Control (skinned) | 0.96 ± 0.21 | -- | -- |
| Rp-8-pCPT-cGMPs(0.5 mM) | 0.48 ± 0.08 | 0.50 | 0.05 |
In experiments 2 and 4, the skin overlying trunk myotomes was removed by suction at stage 24. Embryos were exposed to 8-Br-cGMP or inhibitor in 0.1X MBS (unskinned) or 1X MBS (skinned) from stage 24 until stage 31, when they were fixed for labeling of AChRs with α-bungarotoxin and subsequent confocal microscopy. Each type of experiment was performed 2–4 times.