The relative role of recapture and of de novo synthesis for the maintenance of neurotransmitter homeostasis in noradrenergic nerves.

Abstract

AbstractExperiments were carried out in the isolated, perfused cat spleen to assess the capacity of the mechanisms of synthesis of noradrenaline to keep pace with the loss of noradrenaline by overflow from the organ, during prolonged periods of electrical nerve stimulation. The organ was pretrcated with the monoamine oxidase inhibiting drug nialamide to block deamination of noradrenaline. Phenoxybenzamine or cocaine+ Hydergin were added to the perfusion fluid in order to inhibit reuptake of noradrenaline liberated from the nerves, and to facilitate washout of noradrenaline in the extracellular fluid by preventing the vasoconstriction response. De novo synthesis of noradrenaline was found to proceed at a rate comparable to the highest values described in the literature. However, the discharge of noradrenaline from the neurons in response to nerve stimulation, as reflected by the peak overflow of noradrenaline from the organ, occurred at an approximately ten times higher rate. The results imply that the major mechanism for the maintenance of a constant noradrenaline level in the neuron from one moment to the next, during periods of increased nerve activity, is not de novo synthesis, but rather an almost quantitative reuptake of the noradrenaline liberated from the neurons.