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1.
Ann Thorac Surg ; 95(2): 465-70, 2013 Feb.
Article in English | MEDLINE | ID: mdl-23219256

ABSTRACT

BACKGROUND: The pathophysiologic characteristics of primary hyperhidrosis are not well understood and seem to be related to a sympathetic nervous system dysfunction. The resection of thoracic sympathetic chain ganglia is the most effective treatment for hyperhidrosis; however sympathetic ganglia function in normal individuals and in patients with hyperhidrosis is unknown. METHODS: A cross-sectional study, in which 2 groups of 20 subjects were analyzed: the hyperhidrosis group (HYP), comprised of patients with hyperhidrosis who were eligible for thoracic sympathectomy, and the control group (CON) comprised of brain-dead organ donors without a history of hyperhidrosis. For each subject, the following were performed: resection of the third left sympathetic ganglion, measurement of the ganglion's diameter, and immunohistochemical evaluation by quantification of strong and weak expression areas of primary antibodies against acetylcholine and alpha-7 neuronal nicotinic receptor subunit. RESULTS: The presence of a strong alpha-7 subunit expression area was 4.85% in patients with primary hyperhidrosis and 2.34% in controls (p < 0.001), whereas the presence of a weak expression area was 11.48% in the HYP group and 4.59% in the CON group (p < 0.001). Strong acetylcholine expression was found in 4.95% of the total area in the HYP group and in 1.19% in the CON group (p < 0.001), whereas weak expression was found in 18.55% and 6.77% of the HYP and CON groups, respectively (p < 0.001). Furthermore, diameter of the ganglia was 0.71 cm in the HYP group and 0.53 cm in the CON group (p < 0.001). CONCLUSIONS: There is a higher expression of acetylcholine and alpha-7 neuronal nicotinic receptor subunit in the sympathetic ganglia of patients with hyperhidrosis. Furthermore, the diameter of the thoracic sympathetic chain ganglia is larger in such patients.


Subject(s)
Acetylcholine/biosynthesis , Ganglia, Sympathetic/metabolism , Hyperhidrosis/metabolism , Receptors, Cholinergic/biosynthesis , Adult , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Young Adult
2.
Muscle Nerve ; 38(6): 1585-94, 2008 Dec.
Article in English | MEDLINE | ID: mdl-19016551

ABSTRACT

The absence of dystrophin in Duchenne muscular dystrophy (DMD) and in the mutant mdx mouse causes muscle degeneration and disruption of the neuromuscular junction. Based on evidence from the denervation-like properties of these muscles, we assessed the ligand-binding constants of nicotinic acetylcholine receptors (nAChRs) and the mRNA expression of individual subunits in membrane preparations of diaphragm muscles from adult (4-month-old) and aged (20-month-old) control and mdx mice. The concentration of nAChRs as determined by the maximal specific [(125)I]-alpha-bungarotoxin binding (Bmax) in the muscle membranes did not change with aging in both animal strains. When compared to age-matched control groups, the Bmax in mdx muscles was increased by 65% in adults, and by 103% in aged mice with no alteration of toxin affinity for nAChRs. Reverse-transcription polymerase chain reaction assays showed that mRNA transcripts for the nAChR alpha1, gamma, alpha7, and beta2, but not the epsilon subunits, were more abundant in mdx than in control muscles. The results indicate increased expression of extrajunctional nAChRs in the mdx diaphragm and reflect impairment of nAChR regulation in dystrophin-deficient muscles. These observations may be related to the resistance to nondepolarizing muscle relaxants and the high sensitivity to depolarizing agents reported in DMD patients.


Subject(s)
Diaphragm/metabolism , Receptors, Cholinergic/biosynthesis , Receptors, Cholinergic/genetics , Animals , Bungarotoxins , Data Interpretation, Statistical , Immunohistochemistry , Male , Mice , Mice, Inbred C57BL , Mice, Inbred mdx , Reverse Transcriptase Polymerase Chain Reaction
3.
Rev. chil. anat ; 14(1): 17-22, 1996. ilus, tab
Article in Spanish | LILACS | ID: lil-189276

ABSTRACT

La neurogénesis de las células colinoceptivas que expresan receptores nicotínicos colinérgicos en la retina de pollo, fue estudiada mediante técnica inmunohistoquímica por doble marcación con el anticuerpo monoclonal anti bromodeoxy-uridine (BRDU), que marca los núcleos de las células y con el anticuerpo monoclonal anti receptores nicotínicos colinérgicos (nAChR), que marca el citoplasma de las células. La génesis de esta población neuroniana se produce durante el día embrionario cinco (E-5), iniciándose en la región central de la retina, en la capa nuclear interna, para luego progresar hacia la capa ganglionar y regiones más periféricas de la retina.


Subject(s)
Chick Embryo , Animals , Receptors, Cholinergic/biosynthesis , Retinal Ganglion Cells/physiology , Cholinergic Agents , Bromodeoxyuridine , Chick Embryo/cytology , Receptors, Cholinergic/physiology , Receptors, Nicotinic/biosynthesis , Retinal Ganglion Cells/cytology
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