Activation of NK1 receptor of trigeminal root ganglion via substance P paracrine mechanism contributes to the mechanical allodynia in the temporomandibular joint inflammation in rats

• Published in: Pain (Amsterdam) Vol. 116; no. 3; pp. 375 - 385
• Main Authors: Takeda, Mamoru, Tanimoto, Takeshi, Nasu, Masanori, Ikeda, Mizuho, Kadoi, Jun, Matsumoto, Shigeji
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 01.08.2005; Elsevier
• Subjects: Action Potentials - drug effects; Action Potentials - physiology; Animals; Behavior, Animal; Biological and medical sciences; Cell Count; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction; Dose-Response Relationship, Drug; Drug Interactions; Escape Reaction - drug effects; Escape Reaction - physiology; Freund's Adjuvant; Functional Laterality - physiology; Fundamental and applied biological sciences. Psychology; Inflammation; Iontophoresis; Male; Medical sciences; Models, Biological; Nervous system (semeiology, syndromes); Neural Conduction - drug effects; Neural Conduction - physiology; Neural Conduction - radiation effects; Neurology; Neurons - drug effects; Neurons - physiology; NK1 receptor; Nociceptors - metabolism; Pain Threshold - drug effects; Pain Threshold - physiology; Paracrine; Paracrine Communication - drug effects; Paracrine Communication - physiology; Physical Stimulation - methods; Quinuclidines - pharmacology; Rats; Rats, Wistar; Receptors, Neurokinin-1 - physiology; Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors; Substance P; Substance P - metabolism; Temporomandibular Joint Disorders - chemically induced; Temporomandibular Joint Disorders - complications; Temporomandibular Joint Disorders - metabolism; Temporomandibular Joint Disorders - physiopathology; Trigeminal Ganglion - pathology; Trigeminal root ganglion; Vertebrates: nervous system and sense organs; Paracrine; Iontophoresis; Inflammation; Trigeminal root ganglion; NK1 receptor; Substance P; Rat; Diseases of the osteoarticular system; Electrophysiology; Temporomandibular joint; Neuropeptide; Temporomandibular joint dysfunction; Osteoarticular system; Electrodes; Maxillary disease; Allodynia; NK1 Tachykinin receptor; Stomatology; Electrical stimulus; Rodentia; Discharge pattern; Excitability; Vertebrata; Mammalia; Neuron; Pentobarbital; Arthropathy; Skin; Trigeminal ganglion; Tachykinin
• ISSN: 0304-3959; 1872-6623
• DOI: 10.1016/j.pain.2005.05.007

The aim of this study was to investigate whether under in vivo conditions, temporomandibular joint (TMJ) inflammation alters the excitability of Aβ-trigeminal root ganglion (TRG) neuronal activity innervating the facial skin by using extracellular electrophysiological recording with multibarrel-electrodes. Complete Freund's adjuvant (CFA) was injected into the rat TMJ. Threshold for escape from mechanical stimulation applied to the whisker pad area in inflamed rats (2 days) was significantly lower than that in control rats. A total of 36 Aβ-TRG neurons responding to electrical stimulation of the whisker pad was recorded in pentobarbital-anesthetized rats. The number of Aβ-TRG neurons with spontaneous firings and their firing rate in TMJ inflamed rats were significantly larger than those in control rats. The firing rates of their spontaneous activity in the Aβ-TRG neurons were current-dependently decreased by local iontophoretic application of an NK1 receptor antagonist (L-703,606) in inflamed, but not non-inflamed rats. Their spontaneous activities were current-dependently increased by local iontophoretic application of substance P (SP) in control and inflamed rats. The mechanical response threshold of Aβ-TRG neurons in inflamed rats was significantly lower than that in control rats. The mechanical response threshold in inflamed rats after iontophoretic application of L-703,606 was not different from that in control rats. These results suggest that TMJ inflammation modulate the excitability of Aβ-TRG neurons innervating the facial skin via paracrine mechanism due to SP released from TRG neuronal cell body. Such a SP release may play an important role in determining the trigeminal inflammatory allodynia concerning the temporomandibular disorder.