Simultaneous depletion of neurokinin A, substance P and calcitonin gene-related peptide from the caudal trigeminal nucleus of the rat during electrical stimulation of the trigeminal ganglion.

The central terminals of the primary sensory trigeminal ganglion (TG) neurons projecting into the caudal trigeminal nucleus (CTN) of the rat exhibit neurokinin A (NKA)-, substance P (SP)-, and calcitonin gene-related peptide (CGRP)-immunoreactivities (IRs). We stimulated the TG in the rat to induce some of the alterations which might occur during migraine (neurogenic inflammation). Under a stereotaxic apparatus and by means of a bipolar electrode, one-side TG of the animals were electrically stimulated (7.5 Hz, 5 ms, 0.8-1. 4 mA) with square pulses for 5 min. Then, using immunohistochemical methods, the lower medulla of each rat was studied for NKA-, SP- and CGRP-IRs. Light microscopic examination of brain-stem sequencial sections revealed a simultaneous decrease in the immunoreactivities of all neuropeptides (NKA, SP and CGRP) in the CTN ipsilateral to TG stimulation in comparison with the other (not stimulated) side CTN. It is suggested that this decrease in immunoreactivity would be due to the co-release of neuropeptides following noxious stimuli and that NKA, SP and CGRP might therefore act as co-transmitters or co-modulators at the first central synapses of the trigeminal sensory pathway.