Dystrophin Stabilizes α3- But Not α7-Containing Nicotinic Acetylcholine Receptor Subtypes at the Postsynaptic Apparatus in the Mouse Superior Cervical Ganglion

Abstract

The nicotinic acetylcholine receptor (nAChR) subtypes were characterized in the superior cervical ganglion (SCG) of wild-type and dystrophin-lacking mdx mice. The binding of Epibatidine and αBungarotoxin, ligands for α3- and α7-containing receptors, respectively, revealed, for each ligand, a single class of high-affinity binding sites, with similar affinity in both wild-type and mdx mice. The Epibatidine-labeled receptors were immunoprecipitated by antibodies against the α3, β2, and β4 subunits. Immunocytochemistry showed that the percentage of α3-, β2-, and β4- but not of α7-immunopositive postsynaptic specializations was significantly lower in mdx than in wild-type mouse SCG. These observations suggest that the mouse SCG contains nAChRs, stabilized by dystrophin, in which the α3 subunit is associated with the β2 and/or β4 subunits. Conversely, dystrophin is not involved in the stabilization of the α7-containing nAChRs, as the percentage of α7-immunopositive synapses is similar in both wild-type and mdx mouse SCG.

Keywords

• αbungarotoxin
• dystrophin-dystroglycan complex
• epibatidine
• genetically dystrophic mdx mice
• immunoelectron microscopy
• neuronal nicotinic acetylcholine receptor subtypes