Increased axonal transport of trigeminal ganglion proteins in an electrode model.

This investigation uses an electrical stimulation model of ocular herpes simplex virus (HSV) reactivation to elucidate the relationship between neuronal protein synthesis, axonal transport and electrical stimulation. In this study, healthy adult albino rabbits were implanted with electrodes over the trigeminal ganglion (TG) and stimulated chronically twice a week for 28-34 days (previously shown to induce HSV reactivation in infected rabbits). The TG was visualized surgically and injected with 3H-proline to label newly synthesized protein. After various times, the TG, corneas and ophthalmic nerve were analyzed for labeled proteins. In nonimplanted and implanted rabbits (whether stimulated or not), the rate of fast anterograde axonal transport in the ophthalmic nerve was 347 mm/day and 326 mm/day, respectively. A lag period of 45 min occurred between initiation of protein labeling and onset of axonal transport. Only a small percentage of newly synthesized neuronal proteins were transported in the ophthalmic nerve (1-4% in the proximal 10 mm) or deposited in the cornea (less than 0.5%) after 24 hr. Neither the rate of protein synthesis in the TG nor the rate of axonal transport was changed by electrical stimulation. However, the amount of radioactively labeled proteins undergoing axonal transport in the stimulated group was five times that of the sham control group. Thus, the routing and loading of TG proteins for axonal transport is enhanced in the electrical stimulation model.