Facial-facial anastomosis (FFA), i.e., suture of transected facial nerve, was performed in adult Wistar rats. For 10-112 d post-operation (DPO), half of the animals received standard food (placebo) and half received food pellets containing 1000 ppm nimodipine, a Ca2+ channel blocker. The time course of mimetic reinnervation between these two groups was compared by counting all retrogradely labeled motoneurons after injection of horseradish peroxidase (HRP) into the whiskerpad. In unoperated animals, injection of HRP labeled 1280 +/- 113 motoneurons. After FFA, this number dropped to zero, and the first HRP-labeled facial motoneurons reappeared in both placebo- and nimodipine-treated animals at 14 DPO. The treatment with nimodipine yielded two beneficial effects. (1) It accelerated axonal sprouting until 28 DPO. Whereas the number of HRP-labeled cells in the placebo group was 171 +/- 9 (mean +/- SD) at 16 DPO, 372 +/- 43 at 21 DPO, and 636 +/- 187 at 28 DPO, the number of sprouted motoneurons in nimodipine-treated rats was twice as high: 386 +/- 34 at 16 DPO, 620 +/- 28 at 21 DPO, and 756 +/- 257 at 28 DPO. (2) Nimodipine reduced the polyneuronal innervation of the target muscles. Whereas the number of HRP-labeled cells in the placebo group increased to 1430 +/- 36 at 56 DPO and 1600 +/- 31 at 112 DPO, the number of labeled motoneurons in nimodipine-treated rats remained almost within the normal range: 1315 +/- 31 at 56 DPO and 1354 +/- 33 at 112 DPO.

Therapeutic vaccination with Copaxone (glatiramer acetate, Cop-1) protects motor neurons against acute and chronic degenerative conditions. In acute degeneration after facial nerve axotomy, the number of surviving motor neurons was almost two times higher in Cop-1-vaccinated mice than in nonvaccinated mice, or in mice injected with PBS emulsified in complete Freund's adjuvant (P < 0.05). In mice that express the mutant human gene Cu͞Zn superoxide dismutase G93A (SOD1), and therefore simulate the chronic human motor neuron disease amyotrophic lateral sclerosis, Cop-1 vaccination prolonged life span compared to untreated matched controls, from 211 ؎ 7 days (n ‫؍‬ 15) to 263 ؎ 8 days (n ‫؍‬ 14; P < 0.0001). Our studies show that vaccination significantly improved motor activity. In line with the experimentally based concept of protective autoimmunity, these findings suggest that Cop-1 vaccination boosts the local immune response needed to combat destructive self-compounds associated with motor neuron death. Its differential action in CNS autoimmune diseases and neurodegenerative disorders, depending on the regimen used, allows its use as a therapy for either condition. Daily administration of Cop-1 is an approved treatment for multiple sclerosis. The protocol for non-autoimmune neurodegenerative diseases such as amyotrophic lateral sclerosis, remains to be established by future studies.

The ability of the facial motor system to adapt to a new motor function was studied in alert cats after unilateral transection, 180 degrees rotation and suture of the zygomatic nerve, or transection and cross-anastomosis of the proximal stump of the buccal nerve to the distal stump of the zygomatic nerve. These procedures induced reinnervation of the orbicularis oculi (OO) muscle by different OO- or mouth-related facial motoneurons. Eyelid movements and the electromyographic activity of the OO muscle were recorded up to 1 year following the two types of anastomosis. Animals with a zygomatic nerve rotation recovered spontaneous and reflex responses, but with evident deficits in eyelid kinematics, i.e. the proper regional distribution of OO motor units was disorganized by zygomatic nerve rotation and resuture, producing a permanent defect in eyelid motor performance. Following buccal-zygomatic anastomosis, the electrical activity of the OO muscle was recovered after 6-7 weeks, but air puff-, flash- and tone-evoked reflex blinks never reached the control values on the operated side. Electromyographic OO activities and lid movements corresponding to licking and deglutition activities were observed on the operated side in buccal-zygomatic anastomosed animals up to 1 year following surgery. Mouth-related facial motoneurons did not readapt their discharges to the kinetic, timing and oscillatory properties of OO muscle fibres. A significant hyper-reflexia was observed following both types of nerve repair in response to air puffs, but not to light flashes or tones. In conclusion, adult mammal facial premotor circuits maintain their motor programmes when motoneurons are induced to reinnervate a foreign muscle, or even a new set of muscle fibres.