Nimodipine-accelerated hypoglossal sprouting prevents the postoperative hyperinnervation of target muscles after hypo glossal-facial anastomosis in the rat.

Hypoglossal-facial anastomosis (HFA), used for the treatment of facial palsy, was performed in adult Wistar rats. For 7-224 days post operation (DPO), half of the animals were kept on standard laboratory food and half received food pellets containing 1000 ppm of the Ca2+ channel blocker nimodipine. The postoperative neurotization of facial muscles in these two groups was traced by comparing numbers of all retrogradely labeled neurons after injection of HRP into the whiskerpad muscles. In unoperated animals, injection of HRP labeled 1254 ± 54 neurons. Immediately after HFA, this number dropped to zero. The treatment with nimodipine yielded two beneficial effects. (1) In the early phase of regeneration (until 28 DPO), it accelerated the sprouting of hypoglossal axons into the facial periphery; (2) In the final phase, it suppressed the axonal sprouting from both, hypoglossal and facial stumps. In this way nimodipine fully prevented the postoperative hyperinnervation, i.e. the projection of more hypoglossal plus facial motoneurons to the whiskerpad muscles than under normal conditions.