Abstract

A decussation of histamine (HA)-containing nervous pathways, at the level of the sympathetic ganglionic clusters of the rat vas deferens, was formerly described in this laboratory. This type of neuronal distribution is confirmed in the present study by using surgical interruptions of nervous pathways and determining changes in L-histidine decarboxylase (HD) activity, as an HA-containing neuron marker, after nerve degeneration. Decreases of HD activity follow previously found decreases of HA levels in the vas deferens submitted to the same type of surgical interruptions. An interaction between noradrenergic neurons and HA-containing neurons is suggested, because electrical stimulation of the preganglionic sympathetic nerve causes a rapid increase in HD activity in the ipsilateral vas deferens, possibly as a signal of the activation of HA-containing neurons, whose pathways come from the opposite ganglion. This activation appears to be indirect, presumably through a sensory interneuron, which upon being excited by the enhanced sympathetic discharge crosses over to stimulate the contralateral ganglionic HA-containing neuron. The sympathetic discharge-induced peripheral loop reflex resulting in an increase in HD activity depends upon the integrity of the noradrenergic neuron. An, as yet unknown, interaction seems to occur between the noradrenergic neurons and the HA-containing neurons in the rat vas deferens, when the sympathetic activity of the latter is enhanced.