Booj_1981_J.Neural.Transm_52_213

The influence of descending bulbospinal monoamine (MA) neurons on the intra-axonal transport of acetylcholine (ACh) and related enzymes (cholineacetyltransferase, CAT, and ACh-esterase, AChE) in rat sciatic nerve was studied in crush experiments following intracisternal injections of specific neurotoxins. The injection of 6-hydroxydopamine (6-OH-DA) and 5,6-dihydroxytryptamine (5,6-diOH-TA) (50 micrograms X 2) caused a degeneration of catecholamine (CA) and 5-hydroxytryptamine (5-HT) nerve terminals, respectively, and a combination of the two neurotoxins caused a loss of virtually all MA terminals in the lumbar spinal cord. The results of the neurotoxin injections were controlled by the Falck-Hillarp fluorescence method. The effect of neurotoxin treatment on the enzyme activities in the sciatic nerve was very small. The ACh levels of uncrushed nerves and in nerves proximal to a crush performed 12 hours before dissection decreased following either 6-OH-DA or 5,6-diOH-TA. However, the combination treatment with both 6-OH-DA and 5,6-diOH-TA had no influence on ACh accumulation and transport, as compared to the control group. In a previous study we have shown that mid-thoracic spinal cord transection increased AChE-transport while ACh-transport was decreased. The results of this study indicate that the bulbospinal MA neurons may be involved (perhaps indirectly) i the regulation of ACh levels and transport in motor neurons, but less important for the modulation of the cholinergic enzymes.