Characterization of sensory deficits in TrkB knockout mice.

The sensory deficit in TrkB deficient mice was evaluated by counting the neuronal loss in lumbar dorsal root ganglia (DRG), the absence of sensory receptors (cutaneous--associated to the hairy and glabrous skin - muscular and articular), and the percentage and size of the neurocalcin-positive DRG neurons (a calcium-binding protein which labels proprioceptive and mechanoceptive neurons). Mice lacking TrkB lost 32% of neurons, corresponding to the intermediate-sized and neurocalcin-positive ones. This neuronal lost was accomplished by the absence of Meissner corpuscles, and reduction of hair follicle-associated sensory nerve endings and Merkel cells. The mutation was without effect on Pacinian corpuscles, Golgi's organs and muscle spindles. Present results further characterize the sensory deficit of the TrkB-/- mice demonstrating that the intermediate-sized neurons in lumbar DRG, as well as the cutaneous rapidly and slowly adapting sensory receptors connected to them, are under the control of TrkB for survival and differentiation. This study might serve as a baseline for future studies in experimentally induced neuropathies affecting TrkB positive DRG neurons and their peripheral targets, and to use TrkB ligands in the treatment of neuropathies in which cutaneous mechanoreceptors are primarily involved.

Massive lymphocyte apoptosis in the thymus of functionally deficient TrkB mice.

The occurrence of TrkB in the murine thymus (15-day and 3-month old) was investigated by Northern blot, Western blot and immunohistochemistry. Furthermore, the thymus of 15-day-old mice carrying a non-functional mutation on trkB was analyzed. Both trkB mRNA and 145 kDa TrkB protein were detected. In addition, isolated lymphocytes and stromal cells also expressed this protein. The thymus of homozygous functionally TrkB-deficient animals showed structural and ultrastructural changes consistent with massive death of cortical lymphocytes, confirmed with TUNEL. Present results suggest a role for TrkB in maintaining the survival or preventing massive death of lymphocytes in the mammalian thymus.

S-100 proteins in the human peripheral nervous system.

This article reviews the distribution of S100 proteins in the human peripheral nervous system. The expression of S100 by peripheral glial cells seems to be a distinctive fact of these cells, independently of their localization and their ability to myelinate or not. S100 proteins expressing cells include satellite cells of sensory, sympathetic and enteric ganglia, supporting cells of the adrenal medulla, myelinating and non-myelinating Schwann cells in the nerve trunks, and the Schwann-related cells of sensory corpuscles. In addition, S100 proteins are expressed in peripheral neurons. Most of them express S100alpha protein, and a subpopulation of sensory neurons in dorsal root ganglia contains S100beta protein or S100alpha plus S100beta proteins.

S-100 protein is a selective marker for sensory hair cells of the lateral line system in teleosts.

The distribution of S100 protein in the neuromast of the lateral line system (LLS) was investigated immunohistochemically in alevins of three species of teleosts (Salmo trutta, Salmo salar and Dicentrarchus labrax), using a polyclonal antibody. In both the neuromasts of the canals, as well as in the pit organs, the hair cells, regarded as the specific sensory cells, displayed cytoplasmic immunoreactivity for S100 protein. Conversely, the supporting cells, mantle cells and basal cells were devoid of immunoreaction. These results demonstrate for the first time the occurrence of S100 in the LLS of teleosts. Due to the cell specific localization, this protein might serve as a marker for sensory hair cells in neuromasts.

[Changes in the upper airway in patients with sleep obstructive apnea and/or chronic snoring treated with mandibular appliances]. / Cambios en la vía aérea superior de pacientes con apnea obstructiva del sueño y/o roncopatía crónica en tratamiento con posicionadores mandibulares.

We have analysed the possible modifications in the upper airways (UA) of the lateral cranial teleradiography in 25 adult males with Obstructive Sleep Apnea (OSAS) and/or chronic snoring, with dental and squeletal Class I, treated with advance mandibular appliances (MAD). Results of our study showed a clear increase of the UA in the oropharynx in all the subjects studied. The study of the changes in the UA using the lateral cranial teleradiography in order to evaluate the effectiveness of the MAD can contribute to consider its effectiveness in the cases with OSAS when they are indicated. However it will be needed to contrast these results with polisomnography.

Postnatal developmental changes in the expression of ErbB receptors in murine Pacinian cospucles.

Neuregulins and their signaling ErbB receptors play a critical role during the development of the mammalian peripheral nervous system, including some kinds of mechanoreceptors such as the Pacinian corpuscles which become structurally and functionally mature postnatally. In this study, we investigated whether or not ErbBs in Pacinian corpuscles undergoes developmental changes, as well as if their expression depends on the innervation. Pacinian corpuscles from 7-day- and 3-month-old mice were assessed for the immunohistochemical detection of EGFR or ErbB1, ErbB2, ErbB3 and ErbB4. The effect of denervation on the expression of ErbBs in mature Pacinian corpuscles was also analyzed. Developing 7-day-old Pacinian corpuscles express ErbB2 and ErbB3 immunoreactivity in the inner-core (regarded as modified Schwann cells), whereas the mature 3-month-old Pacinian corpuscles exclusively displayed ErbB4 immunoreactivity in the outer core and the capsule (regarded as endoneurial and perineurial cells). Denervation was without effect on the ErbB expression. Present results demonstrate maturational related changes and cell segregation in the expression of ErbB receptors by murine Pacinian corpuscles, and that this expression is independent of the innervation.

[Chronic snoring and obstructive sleep apnea-hypopnea syndrome in children]. / Ronchopathie chronique et syndrome de l'apnée-hypopnée obstructive du sommeil chez l'enfant.

The problems children have in sleeping are manifold; the gamut of disorders that have been described ranges from simple, occasional snoring with no accompanying complications, through the syndrome of increased blockage of the upper airways to the obstructive sleep apnea-hypopnea syndrome (OSAHS) where respiratory difficulties accompanied by hypoxemia, hypercapnia and structural sleep difficulties. Mouth breathing and chronic snoring occur frequently in children, with the incidence of snoring, identical for both sexes, varying between 3.2 and 27%. Difficulties in sleeping begin between the ages of the 3 and 9, peaking between 3 and 6. These results demonstrate, in a general way, the disparity between growth of the adenoids and tonsils, and upper airway growth. A differential diagnosis between the various pathological possibilities is based on the observed clinical signs and symptoms, analysis of cephalometric radiographs, polysomnography, a nocturnal cardio-respiratory polygraph and a video film taken during sleep. Snoring is the most characteristic sign of OSAHS in children. We do not yet have available any synthetic study that would sum up results of studies of sleep disorders in children. Nevertheless, we can define obstructive sleep apnea in children as the partial or total cessation of nose and mouth breathing for a period double that of the normal respiratory cycle. Classical treatment of children who suffer from severe respiratory difficulties during sleep, after identification of the etiology of the problem, consists of surgical removal of the adenoids or tonsils and, in certain, continuous positive pressure to assist breathing. The authors of this article have worked with 137 patients between the ages of 6 and 9, 77 of whom were chronic snorers with an average age of 7 years 6 months. The average age of the control group of 60 children was 7 years 2 months. We collected clinical data, medical histories, and distributed a questionnaire to determine individual sleep and vigilance behavior of each child in the sample. To complete our evaluation, we made a cephalometric analysis of facial type, antero-postero skeletal pattern, upper airways, and hyoid bone position. The symptom that we encountered most frequently in young chronic snorers was agitated and uneasy sleep, sometimes accompanied by bed-wetting and cervical hyperextension. We often found daytime symptoms of hyperactivity and personality or behavioral problems. Hypertrophy of the adenoids, the adenoidal fascia, and the tonsils were also frequent clinical signs. The cephalometric analyses often showed the patients to be of the dolichocephalic facial type, often with the mandible rotated posteriorly. The children were as likely to be classified as Class II owing to retrognathic mandibles as to be Class III owing to maxillary deficiencies or mandibular excess. At the level of the upper airways, it appears that the development of snoring can be explained by a reduction in the dimensions of the upper pharynges accompanied by an increase in the dimensions of the middle and lower pharynges.