The rat trigeminal nerve was investigated as a model system for axonal transport to identifiable sensory nerve endings. Following stereotaxic injection of [3-H]proline into the ganglion, the distribution of label in protein and other extracts of ligated or unligated infraorbital nerve was measured in replicates at various time intervals from 30 min to 3 days. In unligated nerves the average maximum velocity of somatofugal protein transport was 228 mm/day. Light microscope autoradiography demonstrated rapid intraaxonal transport of radioactive material to nerve endings in molar teeth and vibrissae. The system appears suitable for investigating the fate of axonally transported material at peripheral receptors.

Animals↗

PubMed1975

Neurokinetics of lidocaine in the infraorbital nerve of the rat in vivo: Relation to sensory block.

The kinetics of neural uptake and efflux of lidocaine hydrochloride were studies by means of a standardized technique for blocking the intraorbital nerve of the rat, using a palatal jig. Following injection of 14-C-labeled local anesthetic, groups of ten animals were saccraficed at incipient recovery from sensory block or at othertimes. The nerves were weighed and assayed for radioactivity. The lengths of nerve containing high levels of lidocaine varied inversely with the times elapsed since onset of block. In experiments where a fixed quantity (2 mg) drug was injected, the incidence of block 2 hours later was concentrated-dependent, occuring in 80 per cent of animals after 2 per cent, in 40 per cent after 1 per cent, and in none after 0.5 per cent lidocaine. Epinephrine, 1:200,000, prolonged by 80 per cent the block effected with 0.2 ml of 1 per cent lidocaine. At the onset of recovery the neural contents of lidocaine at the sites of injection were 484 plus or minus 404 ng/mg of nerve in epinephrine-treated nerves, and 274 plus or minus 218 ng/mg in nonepinephrine-treated nerved (N.S., P greater than 0.05). Quantitative comparisons of in-vivo effectiveness of local anesthetic solutions can be made with this technique.

Animals↗

PubMed1975

Lidocaine effects on brain mitochondrial metabolism in vitro.

Both lidocaine and anoxia inhibit rapid axonal transport. In an attempt to elucidate the mechanism of this action of lidocaine, its effect on mitochondrial respiration was studies. The local anesthetic produces a dose-dependent inhibition of oxygen consumption (50 per cent inhibition at 8mM) by porcine brain mitochondria when glutamate, but not when succinate, serves as the substrate. This indicates electron transport is blocked at the NADH dehydrogenase level. Potent uncoupling of oxidative phosphorylation is observed with both substrates. All of the effects are readily reversible upon removal of the anesthetic. It is concluded that lidocaine apparently inhibits rapid axonal transport by depressing oxidative metabolism.

Animals↗

PubMed1975