Preservation of Alpha-3 Neuronal Nicotinic Acetylcholine Receptor Expression in Sympathetic Ganglia After Brain Death.
Summary of "Preservation of Alpha-3 Neuronal Nicotinic Acetylcholine Receptor Expression in Sympathetic Ganglia After Brain Death."
The goal of this study was to evaluate if the immunohistochemical expression of alpha-3 neuronal nicotinic acetylcholine receptor subunit in sympathetic ganglia remains stable after brain death, determining the possible use of sympathetic thoracic ganglia from subjects after brain death as study group. The third left sympathetic ganglion was resected from patients divided in two groups: BD-organ donors after brain death and CON-patients submitted to sympathectomy for hyperhidrosis (control group). Immunohistochemical staining for alpha-3 neuronal nicotinic acetylcholine receptor subunit was performed; strong and weak expression areas were quantified in both groups. The BD group showed strong alpha-3 neuronal nicotinic acetylcholine receptor expression in 6.55% of the total area, whereas the CON group showed strong expression in 5.91% (p = 0.78). Weak expression was found in 6.47% of brain-dead subjects and in 7.23% of control subjects (p = 0.31). Brain death did not affect the results of the immunohistochemical analysis of sympathetic ganglia, and its use as study group is feasible.
Division of Thoracic Surgery, Heart Institute, University of São Paulo, Av. Dr. Eneas de Carvalho Aguiar, 44, 2° andar, 05403-900, São Paulo, São Paulo, Brazil, firstname.lastname@example.org.
This article was published in the following journal.
Name: Molecular neurobiology
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22274960
- DOI: http://dx.doi.org/10.1007/s12035-012-8235-3
Medical and Biotech [MESH] Definitions
Neurotoxic proteins from the venom of the banded or Formosan krait (Bungarus multicinctus, an elapid snake). alpha-Bungarotoxin blocks nicotinic acetylcholine receptors and has been used to isolate and study them; beta- and gamma-bungarotoxins act presynaptically causing acetylcholine release and depletion. Both alpha and beta forms have been characterized, the alpha being similar to the large, long or Type II neurotoxins from other elapid venoms.
Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.
Myasthenic Syndromes, Congenital
A heterogeneous group of disorders characterized by a congenital defect in neuromuscular transmission at the NEUROMUSCULAR JUNCTION. This includes presynaptic, synaptic, and postsynaptic disorders (that are not of autoimmune origin). The majority of these diseases are caused by mutations of various subunits of the nicotinic acetylcholine receptor (RECEPTORS, NICOTINIC) on the postsynaptic surface of the junction. (From Arch Neurol 1999 Feb;56(2):163-7)
Sympathetic Fibers, Postganglionic
Nerve fibers which project from sympathetic ganglia to synapses on target organs. Sympathetic postganglionic fibers use norepinephrine as transmitter, except for those innervating eccrine sweat glands (and possibly some blood vessels) which use acetylcholine. They may also release peptide cotransmitters.
Receptor, Ciliary Neurotrophic Factor
Cell surface receptors for CILIARY NEUROTROPHIC FACTOR. They are heterotrimeric proteins formed by the association of the CILIARY NEUROTROPHIC FACTOR RECEPTOR ALPHA SUBUNIT with the LEUKEMIA INHIBITORY FACTOR RECEPTOR ALPHA SUBUNIT and the CYTOKINE RECEPTOR GP130. Although the receptor regulates neuronal development, it is structurally similar to the cytokine receptor for INTERLEUKIN-6; (RECEPTORS, INTERLEUKIN-6).
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