TARGET REGULATION OF A MOTOR NEURON-SPECIFIC EPITOPE

In the adult rat nervous system, motor neurons are recognized specific ally by a monoclonal antibody, MO-1. Because binding by MO-1 is lost f ollowing axotomy, contact with the target may regulate this' motor neu ron-specific epitope. To test this hypothesis, we examined the recover y of MO-1 immunoreactivity in hypoglossal neurons following unilateral damage to the hypoglossal nerve. During the first week following nerv e crush, neurons in the ipsilateral hypoglossal nucleus lost all immun oreactivity for MO-1. Antibody binding returned with time, and by 4 we eks, 80% of the injured neurons had recovered the MO-1 epitope. Since motor neurons reinnervate their original targets readily following ner ve crush, it appears that MO-1 binding is recovered when motor neurons return to their original target muscles in the tongue. When the hypog lossal nerve was cut and inserted into a foreign muscle nearby (the st ernomastoid muscle), the MO-1 epitope was not detected in the injured neurons, even when examined 6 weeks after surgery. However, if the ste rnomastoid muscle was denervated prior to insertion of the hypoglossal nerve, thus allowing the hypoglossal nerve to synapse with this forei gn target, increasing numbers of hypoglossal neurons reacquired MO-1 i mmunoreactivity with time. Our results suggest that the MO-1 epitope i s only expressed in motor neurons that are in synaptic contact with sk eletal muscle. Thus, a property that distinguishes mature motor neuron s from other neuronal phenotypes appears to be regulated by direct syn aptic interaction with the postsynaptic target.