title: Mechanical stimulation activates small fiber mediated nociceptive responses in the nucleus gigantocellularis.
abstract: We characterized nociceptive discharges induced by mechanical stimulation and the modulating effects of orphanin FQ on noxious responses in the rat brain stem gigantocellular reticular nucleus (Gi). A pressure pulse of constant force and rising rate was delivered by a mechanical stimulator with feedback control, allowing responses to be analyzed statistically. A pressure pulse of 300 g, which evoked C-fiber mediated nerve responses, was delivered to the tail. Two excitatory (45/58) and one inhibitory (13/58) types of extracellular unit discharges were recorded in Gi. One of the excitatory types was a phasic discharge (13/45) elicited at the onset and/or the end of stimulation. Latencies of the phasic discharges (0.104+/-0.1 s) were shorter than those of other type (tonic) discharges (0.43+/-0.2 s). The tonic discharges (32/45), which frequently persisted past the end of stimulation without adaptation, were classified into two groups. The first group of tonic type units (23/45) was high threshold, like nociceptive specific neurons in the primary sensory cortex, while the second group of neurons (9/45) responded to a wide range of stimulus intensities. The mean frequency, response duration and spike numbers gradually increased with stimulus intensity change in all nine neurons. The neurons encode mechanical stimulus intensity with discharge frequency, response duration and evoked spike numbers. Local injection of orphanin FQ (200 ng/2 microl) changed high threshold tonic type spike numbers in a biphasic manner, i.e., there was an early phase suppression (5-30 min, p=0.016) and a late phase enhancement (30-60 min, p=0.027). In contrast, phasic type discharges did not show an altered discharge pattern in response to orphanin FQ. Thus, orphanin FQ affects small fiber-mediated nociceptive responses and may behave as a complex modulator of pain systems in the brain stem.
authors.affiliation: Department of Anesthesiology, Tokyo Women's Medical University, Tokyo, Japan.
authors.forename: Tomonari
authors.initials: T
authors.lastname: Nagata
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Suzuki
authors.forename: Rihui
authors.initials: R
authors.lastname: Zhang
authors.forename: Makoto
authors.initials: M
authors.lastname: Ozaki
authors.forename: Yoriko
authors.initials: Y
authors.lastname: Kawakami
mesh_terms: D000200:Action Potentials; D000818:Animals; D001933:Brain Stem / Q000378:metabolism / Q000503:physiopathology*; D004594:Electrophysiology; D006358:Hot Temperature; D008297:Male; D009474:Neurons / Q000378:metabolism*; D018847:Opioid Peptides / Q000008:administration & dosage / Q000378:metabolism*; D010146:Pain / Q000378:metabolism / Q000503:physiopathology*; D017288:Pain Threshold / Q000187:drug effects; D010812:Physical Stimulation; D051381:Rats; D017208:Rats, Wistar; D013623:Tail; D000097629:Nociceptin
chemical_list: D018847:Opioid Peptides; D000097629:Nociceptin