- Home
- Knowledge Base
- References
Tongue and hypoglossal morphology after intralingual cholera toxin B-saporin injection
Lind LA, Lever TE, Nichols NL (2021) Tongue and hypoglossal morphology after intralingual cholera toxin B-saporin injection. Muscle Nerve 63(3):413-420. doi: 10.1002/mus.27131
Objective: To evaluate tongue morphology and ultrastructural changes in hypoglossal neurons and nerve fibers in an inducible rat model of dysphagia.
Summary: Preliminary results indicate this model may have translational application to a variety of neurodegenerative diseases resulting in tongue dysfunction and associated dysphagia.
Usage: Rats assigned to the CTB-SAP group (n = 10) received 25 μg CTB-SAP to produce hypoglossal motor neuron death.
Related Products: CTB-SAP (Cat. #IT-14)
Exercise is neuroprotective on the morphology of somatic motoneurons following the death of neighboring motoneurons via androgen action at the target muscle
Chew C, Sengelaub DR (2021) Exercise is neuroprotective on the morphology of somatic motoneurons following the death of neighboring motoneurons via androgen action at the target muscle. Dev Neurobiol 81(1):22-35. doi: 10.1002/dneu.22794
Objective: To determine where the necessary site of androgen action is for exercise-driven neuroprotective effects on induced dendritic atrophy.
Summary: Exercise following neural injury exerts a protective effect on motoneuron dendrites, which acts via androgen receptor action at the target muscle.
Usage: Motoneurons innervating the left vastus medialis (VM) muscle were selectively killed by intramuscular injection of cholera toxin-conjugated saporin (CTB-SAP).
Related Products: CTB-SAP (Cat. #IT-14)
Differential mechanisms are required for phrenic long-term facilitation over the course of motor neuron loss following CTB-SAP intrapleural injections.
Borkowski LF, Nichols NL (2020) Differential mechanisms are required for phrenic long-term facilitation over the course of motor neuron loss following CTB-SAP intrapleural injections. Exp Neurol 334:113460. doi: 10.1016/j.expneurol.2020.113460
Objective: To understand the mechanism responsible for this difference in magnitude of phrenic long-term facilitation (pLTF)
Summary: pLTF in 7d CTB-SAP treated rats is elicited primarily through TrkB and PI3K/Akt-dependent mechanisms, whereas BDNF and MEK/ERK-dependent mechanisms induce pLTF in 28d CTB-SAP treated rats.
Usage: Rats received bilateral intrapleural injections of CTB-SAP; 25 μg dissolved in PBS.
Related Products: CTB-SAP (Cat. #IT-14)
Exercise is neuroprotective to motoneuron dendrites following partial motoneuron depletion via a mechanism dependent on androgen receptors at the target muscle
Chew C (2020) Exercise is neuroprotective to motoneuron dendrites following partial motoneuron depletion via a mechanism dependent on androgen receptors at the target muscle. Indiana Univ, Dept Psychol & Brain Sci Thesis.
Related Products: CTB-SAP (Cat. #IT-14)
Respiratory pathology in the Optn-/- mouse model of Amyotrophic Lateral Sclerosis.
McCall AL, Dhindsa JS, Pucci LA, Kahn AF, Fusco AF, Biswas DD, Strickland LM, Tseng HC, ElMallah MK (2020) Respiratory pathology in the Optn-/- mouse model of Amyotrophic Lateral Sclerosis. Respir Physiol Neurobiol 282:103525. doi: 10.1016/j.resp.2020.103525
Summary: Tongue muscle weakness results in dysarthria and dysphagia leading to recurrent aspiration, choking, and aggravation of respiratory disease.
Related Products: CTB-SAP (Cat. #IT-14)
Local riluzole release from a thermosensitive hydrogel rescues injured motoneurons through nerve root stumps in a brachial plexus injury rat model
Fang J, Li L, Zhai H, Qin B, Quan D, Shi E, Zhu M, Yang J, Liu X, Gu L (2020) Local riluzole release from a thermosensitive hydrogel rescues injured motoneurons through nerve root stumps in a brachial plexus injury rat model. Neurochem Res 45(11):2800-2813. doi: 10.1007/s11064-020-03120-0
Summary: The authors refer to a review by Gulino describing two rodent models of motoneuron degeneration were induced by neurotoxics including volkensin and cholera toxin-B saporin, which are able to destroy motoneurons through retrograde transportation.
Related Products: CTB-SAP (Cat. #IT-14)
Exercise promotes recovery after motoneuron injury via hormonal mechanisms.
Chew C, Sengelaub DR (2020) Exercise promotes recovery after motoneuron injury via hormonal mechanisms. Neural Regen Res 15(8):1373-1376. doi: 10.4103/1673-5374.274323
Objective: To describe how exercise is neuroprotective for motoneurons, accelerating axon regeneration following axotomy and attenuating dendritic atrophy following the death of neighboring motoneurons.
Summary: Exercise offers a simple, low barrier-to-entry behavioral intervention which is neuroprotective and pro-regenerative following neural injury.
Usage: Motoneurons innervating the left vastus medialis muscle were selectively killed by intramuscular injection of CTB-SAP (2 μL, 0.1%).
Related Products: CTB-SAP (Cat. #IT-14)
Adenosine 2A receptor inhibition protects phrenic motor neurons from cell death induced by protein synthesis inhibition.
Seven YB, Simon AK, Sajjadi E, Zwick A, Satriotomo I, Mitchell GS (2020) Adenosine 2A receptor inhibition protects phrenic motor neurons from cell death induced by protein synthesis inhibition. Exp Neurol 323:113067. doi: 10.1016/j.expneurol.2019.113067
Objective: To test the hypothesis that A2A receptor antagonism promotes phrenic motor neuron survival and preserves diaphragm function when faced with toxic, neurodegenerative insults that lead to phrenic motor neuron death.
Summary: The authors utilized a novel neurotoxic model of respiratory motor neuron death using intrapleural injections of CTB-SAP. A2A receptors contribute to neurotoxic phrenic motor neuron death, an effect mitigated by A2A receptor antagonism.
Usage: Intrapleural administration of CTB-SAP (25 μg per side) causes: 1) profound phrenic motor neuron death (~5% survival); 2) ~7-fold increase in phrenic motor neuron A2A receptor expression prior to cell death; and 3) diaphragm muscle paralysis (inactive in most rats; ~7% residual diaphragm EMG amplitude during room air breathing).
Related Products: CTB-SAP (Cat. #IT-14)
Renal denervation for treating congenital long QT syndrome: Shortening the QT interval or modulating sympathetic tone?
Kiuchi MG, Chen S, Carnagarin R, Matthews VB, Schlaich MP (2019) Renal denervation for treating congenital long QT syndrome: Shortening the QT interval or modulating sympathetic tone?. Europace 21(11):1755-1756. doi: 10.1093/europace/euz251
Summary: Targeted ablation of cardiac sympathetic neurons (TACSN) through CTB-SAP injection in the left stellate ganglion (LSG), inhibited its activation, improved sympathetic remodelling, and restored cardiac autonomic balance.
Related Products: CTB-SAP (Cat. #IT-14)
Exercise is neuroprotective following partial motoneuron depletion via androgen action at the target muscle
Chew C, Sengelaub DR (2019) Exercise is neuroprotective following partial motoneuron depletion via androgen action at the target muscle. Neuroscience 2019 Abstracts 134.13. Society for Neuroscience, Chicago, IL.
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. Blockade of the androgen receptor at the target muscle prevents the neuroprotective effects on motoneuron dendrites in rats treated with supplemental androgens. We have recently shown that exercise is also neuroprotective on motoneuron dendrites following partial motoneuron depletion, and circulating levels of androgens have previously been shown to increase following exercise. Together, these results suggest that exercise may be neuroprotective via androgen action at the muscle. In the present study, we examine whether blockade of androgen receptors at the target musculature would prevent the neuroprotective effects of exercise on dendrites following partial motoneuron depletion. Motoneurons innervating the vastus medialis muscle in adult male rats were selectively killed by intramuscular injection of cholera toxin-conjugated saporin. Simultaneously, some saporin-injected rats were given implants of the androgen receptor antagonist hydroxyflutamide, either directly at the quadriceps musculature or interscapularly as a systemic control. Following saporin injections, some animals were allowed free access to running wheels 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 untreated males, partial motoneuron depletion resulted in decreased dendritic length in remaining quadriceps motoneurons. Early data suggests that following partial motoneuron depletion, exercised males with androgen receptor blockade at the quadriceps show dendritic lengths that are significantly shorter than those of exercised males with no treatment, while dendritic lengths in exercised males with interscapular implants do not differ from those of exercised animals without implants. These findings suggest that exercise may be protective against dendritic atrophy via androgens binding at the target musculature.
Related Products: CTB-SAP (Cat. #IT-14)