In the last 15 years a role has been ascribed for the medullary dorsal reticular nucleus as a supraspinal pain modulating area. The medullary dorsal reticular nucleus is reciprocally connected with the spinal dorsal horn, is populated mainly by nociceptive neurons and regulates spinal nociceptive processing. Here we analyze the distribution of brain projections from the medullary dorsal reticular nucleus using the iontophoretic administration of the anterograde tracer biotinylated-dextran amine and the retrograde tracer cholera toxin subunit B. Fibers and terminal boutons labeled from the medullary dorsal reticular nucleus were located predominately in the brainstem, although extending also to the forebrain. In the medulla oblongata, anterograde labeling was observed in the orofacial motor nuclei, inferior olive, caudal ventrolateral medulla, rostral ventromedial medulla, nucleus tractus solitarius and most of the reticular formation. Labeling at the pons-cerebellum level was present in the locus coeruleus, A5 and A7 noradrenergic cell groups, parabrachial and deep cerebellar nuclei, whereas in the mesencephalon it was located in the periaqueductal gray matter, deep mesencephalic, oculomotor and anterior pretectal nuclei, and substantia nigra. In the diencephalon, fibers and terminal boutons were found mainly in the parafascicular, ventromedial, and posterior thalamic nuclei and in the arcuate, lateral, posterior, peri- and paraventricular hypothalamic areas. Telencephalic labeling was consistent but less intense and concentrated in the septal nuclei, globus pallidus and amygdala. The well-known role of the medullary dorsal reticular nucleus in nociception and its pattern of brain projections in rats suggests that the nucleus is possibly implicated in the modulation of: (i) the ascending nociceptive transmission involved in the motivational-affective dimension of pain; (ii) the endogenous supraspinal pain control system centered in the periaqueductal gray matter-rostral ventromedial medulla-spinal cord circuitry; (iii) the motor reactions associated with pain.

This NGI model results in laryngeal chronic inflammation without direct mechanical aggression of the mucosa and may contribute to the study of future therapeutic approaches to this pathology.

Etoricoxib is effective in neurogenic laryngitis for limited periods of administration, indicating that selective COX-2 inhibitors should be evaluated in the future.

Vertebrates are capable of producing a variable sound spectrum. In mammals, lissamphibia, and reptiles, the larynx is the vocal organ responsible for sound production, whereas in birds it is produced by the syrinx, an avian organ located at the base of trachea. The distribution of neuromuscular junctions responsible for the fine control of laryngeal muscle (LM) and syringeal muscle (SM), although studied with some detail in human LM, remains mostly unknown in other vertebrates. In the present study, we analyzed the distribution of motor end plates (MEPs) in LM/SM of different vertebrate classes using the histochemical detection of acetylcholinesterase: the thyroarytenoid and cricoarytenoid LM of mammal (human, rat, and rabbit) and cricoarytenoid LM of nonmammalian (frog and avian) species and the tracheobronchial SM of rooster and pigeon. In humans and frogs/avians, MEPs were distributed diffusely along, respectively, the thyroarytenoid-cricoarytenoid and the cricoarytenoid LM fibers, whereas in rats and rabbits, MEPs were concentrated in a transverse band located in the middle of thyroarytenoid and cricoarytenoid muscle fibers. In roosters and pigeons, MEPs were distributed diffusely along SM fibers. The highly diffuse MEP distribution along human thyroarytenoid and cricoarytenoid fibers indicates that these muscles can markedly change their degree of contraction, which may contribute for the large range of different sounds produced by human vocal folds. The same rationale was applied to discuss the possible functional significance of the morphological distribution of MEPs along the LM/SM of the other vertebrates analyzed. Anat Rec Part A 288A:543-551, 2006 Wiley-Liss, Inc.

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