- Home
- Knowledge Base
- References
Neuroprotective effects of exercise on the morphology of somatic motoneurons following the death of neighboring motoneurons.
Chew C, Sengelaub DR (2019) Neuroprotective effects of exercise on the morphology of somatic motoneurons following the death of neighboring motoneurons. Neurorehabil Neural Repair 33(8):656-667. doi: 10.1177/1545968319860485
Objective: To explore whether exercise shows the same neuroprotective effect on induced dendritic atrophy as that seen with androgen treatment.
Summary: Exercise following neural injury exerts a protective effect on motoneuron dendrites comparable to that seen with exogenous androgen treatment.
Usage: Motoneurons innervating the left vastus medialis muscle were selectively killed by intramuscular injection of CTB-SAP (2 μL, 0.1%). Saporin injection reduced the weight of the vastus medialis muscle; exercise had no effect on muscle weight.
Related Products: CTB-SAP (Cat. #IT-14)
A2A and 5‐HT receptors are differentially required for respiratory plasticity over the course of motor neuron loss in intrapleurally CTB-SAP treated rats.
Borkowski LF, Nichols NL (2019) A2A and 5‐HT receptors are differentially required for respiratory plasticity over the course of motor neuron loss in intrapleurally CTB-SAP treated rats. FASEB J 33(1):843.3. Experimental Biology 2019 Meeting Abstracts doi: 10.1096/fasebj.2019.33.1_supplement.843.3
Objective: To investigate the role of serotonin (5-HT) and adenosine 2A (A2A) receptors in respiratory plasticity.
Summary: A2A receptors are necessary for respiratory plasticity early (7d), but 5-HT receptors are required late (28d).
Usage: Bilateral, intrapleural injections of: 1) CTB-SAP (25 μg), or 2) un-conjugated CTB and SAP (control) in rats.
Related Products: CTB-SAP (Cat. #IT-14)
Neuromuscular plasticity in a mouse neurotoxic model of spinal motoneuronal loss.
Gulino R, Vicario N, Giunta MAS, Spoto G, Calabrese G, Vecchio M, Gulisano M, Leanza G, Parenti R (2019) Neuromuscular plasticity in a mouse neurotoxic model of spinal motoneuronal loss. Int J Mol Sci 20(6):1500. doi: 10.3390/ijms20061500
Objective: To use a neurotoxic model of spinal motoneuron depletion, induced by injection of CTB-SAP, to investigate the possible occurrence of compensatory changes in both the muscle and spinal cord.
Summary: Plastic changes in surviving motoneurons produce a functional restoration probably similar to the compensatory changes occurring in disease. These changes could be driven by glutamatergic signaling; astrocytes contacting surviving motoneurons may support this process.
Usage: Mice received 2 injections of CTB-SAP (3 mcg CTB-Sap in 2 mcL PBS) into the medial and lateral left gastrocnemius muscle.
Related Products: CTB-SAP (Cat. #IT-14)
Neuroprotective effects on the morphology of somatic motoneurons following the death of neighboring motoneurons: A role for microglia
Chew C, Kiley B, Sengelaub D (2019) Neuroprotective effects on the morphology of somatic motoneurons following the death of neighboring motoneurons: A role for microglia. Dev Neurobiol 79:131-154. doi: 10.1002/dneu.22652
Related Products: CTB-SAP (Cat. #IT-14)
Mechanisms of compensatory plasticity for respiratory motor neuron death.
Seven YB, Mitchell GS (2019) Mechanisms of compensatory plasticity for respiratory motor neuron death. Respir Physiol Neurobiol 265:32-39. doi: 10.1016/j.resp.2019.01.001
Summary: Discusses recent advances in understanding of mechanisms giving rise to compensatory respiratory plasticity in response to respiratory motor neuron death.
Related Products: CTB-SAP (Cat. #IT-14)
Targeted ablation of cardiac sympathetic neurons improves ventricular electrical remodelling in a canine model of chronic myocardial infarction.
Xiong L, Liu Y, Zhou M, Wang G, Quan D, Shen C, Shuai W, Kong B, Huang C, Huang H (2018) Targeted ablation of cardiac sympathetic neurons improves ventricular electrical remodelling in a canine model of chronic myocardial infarction. Europace 20(12):2036-2044. doi: 10.1093/europace/euy090
Objective: To evaluate the cardiac electrophysiologic effects of targeted ablation of cardiac sympathetic neurons (TACSN) in a canine model of chronic myocardial infarction (MI).
Summary: Targeted ablation of cardiac sympathetic neuron attenuates sympathetic remodelling and improves ventricular electrical remodelling in the chronic phase of MI. These data suggest that TACSN may be a novel approach to treating ventricular arrhythmias.
Usage: 20 μl of CTB-SAP (1.2 mg/ml) was mixed with 4 μl of 3% Evans blue dye to make it visible (CTB-SAP is colorless), ensuring localization within the ganglia. The CTB-SAP/ Evan blue dye solution was slowly and intermittently injected into the left stellate ganglia using a glass micropipette.
Related Products: CTB-SAP (Cat. #IT-14)
Targeted ablation of distal cerebrospinal fluid-contacting nucleus alleviates renal fibrosis in chronic kidney disease.
Qiu M, Li J, Tan L, Zhang M, Zhou G, Zeng T, Li A (2018) Targeted ablation of distal cerebrospinal fluid-contacting nucleus alleviates renal fibrosis in chronic kidney disease. Front Physiol 9:1640. doi: 10.3389/fphys.2018.01640
Objective: To test the hypothesis that distal cerebrospinal fluid-contacting nucleus (dCSF-CNs) might affect the renin-angiotensin system (RAS) in kidney injury progression.
Summary: Less CTB-labeled neurons were found in dCSF-CNs of CTB-SAP-treated rats. Meanwhile, CTB-SAP downregulated AGT, Ang II, AT1R, NOX2, catalase, MCP-1, IL-6, fibronectin, and collagen I, and upregulated ACE2 and Mas receptor. Targeted dCSF-CNs ablation could alleviate renal inflammation and fibrosis in chronic kidney injury.
Usage: CTB-SAP (500 ng) into the lateral ventricles over a 3-min period.
Related Products: CTB-SAP (Cat. #IT-14)
Exercise is neuroprotective following partial motoneuron depletion: Run for your dendrites
Chew C, Sengelaub DR (2018) Exercise is neuroprotective following partial motoneuron depletion: Run for your dendrites. Neuroscience 2018 Abstracts 761.02 / MM11. Society for Neuroscience, San Diego, CA.
Summary: We have previously demonstrated that partial depletion of motoneurons innervating the quadriceps muscles induces dendritic atrophy in remaining motoneurons. Furthermore, systemic treatment with supplemental androgens is neuroprotective and dendritic atrophy following partial motoneuron depletion is attenuated. Circulating levels of androgens have previously been shown to increase following exercise, and exercise has been demonstrated to be neuroprotective in a variety of other neurodegenerative and injury models. Thus, we hypothesized that allowing animals to exercise following partial motoneuron depletion would produce neuroprotective effects similar to treatment with supplemental androgens. Motoneurons innervating the vastus medialis muscle in adult male rats were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Following saporin injections, some animals were allowed free access to a running wheel attached to their home cages. Four weeks later, motoneurons innervating the ipsilateral vastus lateralis muscle were labeled with cholera toxin-conjugated horseradish peroxidase, and dendritic arbors were reconstructed in three dimensions. Compared with intact normal males, partial motoneuron depletion resulted in decreased dendritic length in remaining quadriceps motoneurons. Early data suggests that exercise can completely protect against this dendritic atrophy, with exercised males showing dendritic arbors lengths significantly longer than saporin and testosterone-treated animals, and of similar length to intact normal animals. These findings suggest that exercise may be a viable means of protecting against collateral dendritic atrophy. The upregulation of testosterone release following exercise combined with our previous data showing the neuroprotective effects of androgen treatment suggest that the neuroprotective following exercise may be attributable to systemic androgen upregulation.
Related Products: CTB-SAP (Cat. #IT-14)
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)
Targeted ablation of cardiac sympathetic neurons attenuates adverse post-infarction remodeling and left ventricle dysfunction.
Xiong L, Liu Y, Zhou M, Wang G, Quan D, Shuai W, Shen C, Kong B, Huang C, Huang H (2018) Targeted ablation of cardiac sympathetic neurons attenuates adverse post-infarction remodeling and left ventricle dysfunction. Exp Physiol 103:1221-1229. doi: 10.1113/EP086928
Objective: To determine whether targeted ablation of cardiac sympathetic neurons (TACSN) could suppress myocardial infarction-induced adverse cardiac remodeling and left ventricle dysfunction.
Summary: TACSN significantly alleviated sympathetic remodeling and neuroendocrine activation, attenuated cardiac hypertrophy and fibrosis, and improved the left ventricular function. Thus, TACSN may have a beneficial effect on adverse post-infarction remodeling and left ventricle dysfunction.
Usage: 20 μl of CTB-SAP (1.2 mg/ml) was mixed with 4 μl of 3% Evans blue dye to make it visible (CTB-SAP is colorless), ensuring localization within the ganglia. The CTB-SAP/Evans blue dye solution was slowly and intermittently injected into the left stellate ganglia using a glass micropipette.
Related Products: CTB-SAP (Cat. #IT-14)