The GM1 (Galactosyl-N-Acetylgalactosaminyl) receptor is found on cells such as motoneurons, sympathetic pre-ganglionic neurons, astrocytes as well as cells in the intestinal epithelium. Cholera toxin B (CTB) binds the GM1 receptor and administration of CTB-SAP causes ablation of the specific cells expressing the receptor. CTB-SAP can be used to create a model of respiratory motor neuron death to establish an animal model of Amyotrophic lateral sclerosis (ALS), otherwise known as Lou Gehrig’s disease. This model also demonstrates that CTB-SAP is retrogradely transported. Intrathecal injection of CTB-SAP results in elimination of oligodendrocytes and astrocytes as well as supporting the study of demyelinating conditions.
CTB-SAP is a chemical conjugate of cholera toxin B-subunit and the ribosome-inactivating protein, saporin. It specifically eliminates cells expressing the GM1 receptor, including preganglionic neurons, motoneurons, and astrocytes.
U.S. Patent 6.376,460 “Method of Modulating Cellular Activity” protects methods of peripheral injection of subjects using this neuronal tracer. Before using these methods please contact Flinders Technologies Pty. Ltd. for license information. flinderstech@flinders.edu.au
CTB-SAP is available individually (Cat. #IT-14) or as a kit (Cat. #KIT-14) which includes CTB-SAP and Saporin (Cat. #PR-01).
keywords: GM1 receptor, Cholera Toxin B, ALS, Amyotrophic lateral sclerosis, animal model, lou gehrig’s disease, retrograde transport, astrocytes, demylelinating, oligodendrocytes, motoneurons , preganglionic neurons
Hypoglossal motor neuron death via intralingual CTB-saporin (CTB-SAP) injections mimic aspects of amyotrophic lateral sclerosis (ALS) related to dysphagia
Lind LA, Murphy ER, Lever TE, Nichols NL (2018) Hypoglossal motor neuron death via intralingual CTB-saporin (CTB-SAP) injections mimic aspects of amyotrophic lateral sclerosis (ALS) related to dysphagia. Neuroscience 390:303-316. doi: 10.1016/j.neuroscience.2018.08.026
Objective: Despite its fundamental importance, dysphagia (difficulty swallowing) and strategies to preserve swallowing function have seldom been studied in ALS models.
Summary: The authors report a novel experimental model using intralingual injections of cholera toxin B conjugated to saporin (CTB-SAP) to study the impact of only hypoglossal motor neuron death without the many complications that are present in ALS models.
Usage: Hypoglossal motor neuron survival, swallowing function, and hypoglossal motor output were assessed in Sprague Dawley rats after intralingual injection of either CTB-SAP (25 ug) or unconjugated CTB and SAP (controls) into the genioglossus muscle.
Related Products: CTB-SAP (Cat. #IT-14)
Adenosine 2A receptor inhibition promotes neuroprotection following toxic insult to phrenic motor neurons.
Sajjadi E, Seven YB, Simon AK, Zwick A, Satriotomo I, Mitchell GS (2019) Adenosine 2A receptor inhibition promotes neuroprotection following toxic insult to phrenic motor neurons. FASEB J 33(1):844.3. Experimental Biology 2019 Meeting Abstracts doi: 10.1096/fasebj.2019.33.1_supplement.844.3
Objective: The authors explored the role of A2A receptors in phrenic motor neuron cell death in vivo.
Summary: A2A receptors, which contribute to motor neuron death during toxic insults, are upregulated in spared phrenic motor neurons of CTB-SAP treated rats. This is an important finding since A2A receptor upregulation may accelerate motor neuron death in neurodegenerative diseases like ALS.
Usage: CTB-SAP selectively killed nearly all phrenic motor neurons within a week and caused diaphragm paralysis (p<0.01).
Related Products: CTB-SAP (Cat. #IT-14)
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