Rats were given standardized injections of3H-L-proline into the trigeminal ganglion and14C-lidocaine hydrochloride at the infraorbital foramen. The3H-L-proline was always injected 2.5 h before removal of the nerve. Lidocaine, 1,2, and 4 per cent, produced a concentration-related inhibition of entry of3H-labeled rapid axonal transport into the distal portions of the nerve. Addition of epinephrine, 1:200,000, doubled the intensify of the effect. The time delay of recovery was also concentration-related, and with 4 per cent lidocaine recovery' still seemed incomplete after 4.5 h. It is concluded that inhibition of rapid axonal transport is probably a usual byproduct of nerve block with local anesthetics such as lidocaine. The inhibition seems attributable in part to a disturbance of the energy metabolism of the nerve.