Differential Regulation of Transcripts for Dystrophin Isoforms, Dystroglycan, and α3AChR Subunit in Mouse Sympathetic Ganglia Following Postganglionic Nerve Crush

• Published in: Neurobiology of disease Vol. 8; no. 3; pp. 513 - 524
• Main Authors: Zaccaria, M.L., Perrone-Capano, C., Melucci-Vigo, G., Gaeta, L., Petrucci, T.C., Paggi, P.
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 01.06.2001; Elsevier
• Subjects: axotomy; dystroglycan; dystrophins; neuronal nicotinic acetylcholine receptor; RT-PCR; superior cervical ganglion; superior cervical ganglion; axotomy; dystroglycan; neuronal nicotinic acetylcholine receptor; RT-PCR; dystrophins
• ISSN: 0969-9961; 1095-953X
• DOI: 10.1006/nbdi.2001.0391

Previous data suggest that in mouse superior cervical ganglion (SCG) the dystrophin–dystroglycan complex may be involved in the axotomy-induced intraganglionic synapse remodeling. Here we analyzed the levels of mRNAs encoding dystrophins, dystroglycan (Dg), and the α3 subunit of the nicotinic acetylcholine receptor (α3AChR) in mouse SCG at various postaxotomy intervals. We found that axotomy downregulates the levels of transcripts for molecules related to synaptic transmission (α3AChR) and those presumably involved in postsynaptic apparatus organization (dystrophin isoforms) and upregulates the transcript encoding Dg, which, by binding dystrophin, bridges the actin cytoskeleton and several extracellular matrix proteins and may thus be involved in postaxotomy neuronal recovery. The observed transcriptional modulation of the components of dystrophin–dystroglycan complexes indicates their involvement in injury-induced neuronal plasticity and suggests a role in other forms of plasticity such as those required in learning and memory, functions often impaired in Duchenne muscular dystrophy patients.