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Spinal TNF-α receptor 1 is differentially required for phrenic long-term facilitation (pLTF) over the course of motor neuron death in adult rats
Lewis RD, Keilholz AN, Smith CL, Burd EA, Nichols NL (2024) Spinal TNF-α receptor 1 is differentially required for phrenic long-term facilitation (pLTF) over the course of motor neuron death in adult rats. Front Physiol 15 doi: 10.3389/fphys.2024.1488951 PMID: 39703667
Objective: To study the impact motor neuron death has on the output of surviving phrenic motor neurons as well as the compensatory mechanisms that are recruited.
Summary: Results revealed that TNFR1 expression was increased on phrenic motor neurons of 28d CTB-SAP rats, and that astrocytes were increased and exhibited reactive morphology in the phrenic motor nucleus of CTB-SAP rats. This work suggests that TNFR1 could be used as a potential therapeutic agent in CTB-SAP rats and patients with respiratory motor neuron disease.
Usage: Intrapleural injection of CTB-SAP (25μg dissolved in PBS) to target respiratory motor neurons.
Related Products: CTB-SAP (Cat. #IT-14)
Tongue exercise ameliorates structural and functional upper airway deficits in a rodent model of hypoglossal motor neuron loss
Keilhoz A, Pathak I, Smith CL, Osman KL, Smith L, Oti G, Golzy M, Mz L, Lever TE, Nichols NL (2024) Tongue exercise ameliorates structural and functional upper airway deficits in a rodent model of hypoglossal motor neuron loss. Front Neurol 15:1441529. doi: 10.3389/fneur.2024.1441529 PMID: 39296960
Objective: To investigate the effects of a strength endurance tongue exercise program on upper airway structure and function.
Summary: Results showed that sham exercise-treated CTB-SAP rats have evidence of upper airway restriction (i.e., reduced airflow) and structural changes present in the upper airway (i.e., airway compression) when compared to rats treated with CTB-SAP and exercise and control rats with/without tongue exercise, which were ameliorated with tongue exercise. Additionally, CTB-SAP treated, sham exercise rats have evidence of increased lipid expression in the tongue consistent with previously observed tongue hypertrophy when compared to CTB-SAP treated exercise rats or control rats with/without tongue exercise.
Usage: Intralingual injection of either unconjugated CTB+SAP (20 μg CTB+25 μg SAP) or conjugated CTB-SAP (25 μg of CTB conjugated to SAP).
Related Products: CTB-SAP (Cat. #IT-14), Recombinant Cholera Toxin B (Cat. #PR-14), Saporin (Cat. #PR-01)
Mitigating the functional deficit after neurotoxic motoneuronal loss by an inhibitor of mitochondrial fission
Ciuro M, Sangiorgio M, Cacciato V, Cantone G, Fichera C, Salvatorelli L, Magro G, Leanza G, Vecchio M, Valle MS, Gulino R (2024) Mitigating the functional deficit after neurotoxic motoneuronal loss by an inhibitor of mitochondrial fission. Int J Mol Sci 25(13):7059. doi: 10.3390/ijms25137059 PMID: 39000168
Objective: To use the Cholera Toxin B-Saporin (CTB-SAP) mouse animal model of Amyotrophic lateral sclerosis (ALS) to determine the efficacy of mitochondrial division inhibitor 1 (Mdivi-1) for its potential neuroprotective effect.
Summary: Mdivi-1 reduced motor deficits in the ALS model. It also showed neuroprotective effects on motoneurons and promoted plasticity. This could represent a translational approach for motoneuron disorders.
Usage: To establish the model, mice received two injections of the retrogradely transported, ribosome-inactivating toxin, CTB-SAP (Cat. #IT-14) into the medial and lateral right gastrocnemius muscles, respectively, with a toxin dose of 6 μg/2 μL in PBS per injection.
Related Products: CTB-SAP (Cat. #IT-14)
Longitudinal assessment of outcome measures of diaphragm motor unit connectivity as biomarkers of phrenic motor unit degeneration and compensation
Ketabforoush A, Wang M, Smith C, Arnold WD, Nichols N (2024) Longitudinal assessment of outcome measures of diaphragm motor unit connectivity as biomarkers of phrenic motor unit degeneration and compensation. Am Physiol Summit 39(S1) doi: 10.1152/physiol.2024.39.S1.1402
Objective: Using CTB-SAP to lesion motor neurons and measuring motor neuron connectivity and cell death, as a model for phrenic motor neuron degeneration.
Summary: Processes such as injury or aging can affect motor neurons and cause degeneration. CTB-SAP is used to mimic this phenomenon and is used to cause motor degeneration in the diaphram of rats. The motor neurons and motor units have plasticity and the ability to compensate for this damage and the authors seek to use the created rat model to measure this motor unit connectivity.
Usage: Rats received bilateral intrapleural injections of 25 μg of CTB-SAP (IT-14) as well as 25 more μg of free CTB. Control mice received 25 μg of free saporin and 25 μg of CTB.
Related Products: CTB-SAP (Cat. #IT-14)
Activation of alpha 2 adrenergic receptor of cerebrospinal fluid-contacting nucleus alleviates acute incision pain behavior in rats
Meng XT, Song SY, Li Y, Peng S, Zhang LC (2024) Activation of alpha 2 adrenergic receptor of cerebrospinal fluid-contacting nucleus alleviates acute incision pain behavior in rats. Research Square doi: 10.21203/rs.3.rs-4258857/v1
Objective: To study the effects of Dexmedetomidine (DEX) on pain modulation.
Summary: Dexmedetomidine is an alpha 2-adrenergic receptor agonist with sedative, analgesic, and anti-anxiety effects. DEX was analyzed for its effects using a pain neuron knockout model of rats created by ablation of cerebrospinal fluid contacting neurons in the lateral ventricles of rats. DEX inhibited the pain behavior of rats in a dose-dependent manner, and the analgesic effect of DEX was significantly attenuated in CSF-contacting nucleus “knockout” rats.
Usage: CTB-SAP [IT-14] (0.5 µg in 3 µL) was injected into the lateral ventricles (L.V.) of rats over 10 minutes.
Related Products: CTB-SAP (Cat. #IT-14)
Unveiling cholera toxin binding and intoxication using enteroids and site-specific mutants
Boucher A (2024) Unveiling cholera toxin binding and intoxication using enteroids and site-specific mutants. Univ Gothenburg Thesis.
Objective: To investigate the binding site requirements of cholera toxin in the human body.
Summary: The cause of cholera symptoms is cholera toxin secreted by bacteria once in the small intestine. Cholera toxin has multiple binding sites that lead to many different intake mechanisms. By identifying the binding sites responsible, the study seeks to lay the groundwork for better means of treatment.
Usage: Leukocytes were treated with biotinylated Cholera toxin B binding-deficient mutants mixed with Streptavidin-SAP (IT-27) and assessed for cell death.
Related Products: CTB-SAP (Cat. #IT-14), Streptavidin-ZAP (Cat. #IT-27), Recombinant Cholera Toxin B (Cat. #PR-14)
Autonomic nerve and its modulation approaches for heart failure
Zhang H, Zhu Y, Chen S, Deng K, Zheng M, Zeng Z, Wang Q, Cai H, Lu Z (2023) Autonomic nerve and its modulation approaches for heart failure. Brain & Heart 1(2):0913. doi: 10.36922/bh.0913
Objective: Authors review neural modulation approaches that can assist in the management of heart failure.
Summary: The autonomic nervous system governs the heart’s neurological regulation through opposing functions of its sympathetic and parasympathetic components. Potential treatments for heart failure include inhibiting the sympathetic nerve’s overactivity and restoring parasympathetic activity in the heart. CTB-SAP was used to ablate cardiac sympathetic neurons via retrograde transport on stellate ganglion neurons.
Usage: CTB-SAP was injected into the right superior vervical ganglion of adult male Sprague-Dawley rats (50 ug/rat).
Related Products: CTB-SAP (Cat. #IT-14)
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Tongue exercise-induced functional and structural upper airway plasticity in a rodent model of hypoglossal (XII) motor neuron loss
Keilholz A, Homan C, Schroeder A, Osman K, Smith C, Pathak I, Streeter K, Ozden I, Ma L, Lever T, Nichols N (2023) Tongue exercise-induced functional and structural upper airway plasticity in a rodent model of hypoglossal (XII) motor neuron loss. American Physiology Summit 2023 Meeting Abstracts 38(S1)
Objective: Examine if upper airway function/coordination can be improved in lower motor neuron (LMN) degeneration by tongue exercise-induced axis plasticity.
Summary: Tongue muscle weakness in patients with motor neuron diseases suggests a potential role for therapeutic exercise but lacks evidence due to lack of an appropriate model. Data suggests that tongue exercise in CTB-SAP rats results in enhanced XII motor plasticity and mitigates structural airway changes. In conclusion, tongue exercise appears to cause XII-tongue axis plasticity to improve upper airway function and coordination in the face of XII LMN degeneration.
Usage: The authors developed a novel rodent model using intralingual injections of CTB-SAP to induce targeted loss of XII motor neurons and motor output.
Related Products: CTB-SAP (Cat. #IT-14)
A strength endurance exercise paradigm mitigates deficits in hypoglossal-tongue axis function, strength, and structure in a rodent model of hypoglossal motor neuron degeneration
Murphy ER, Thompson R, Osman KL, Haxton C, Brothers M, Lee L, Warncke K, Smith CL, Keilholz AN, Hamad A, Golzy M, Bunyak F, Ma L, Nichols NL, Lever TE (2022) A strength endurance exercise paradigm mitigates deficits in hypoglossal-tongue axis function, strength, and structure in a rodent model of hypoglossal motor neuron degeneration. Front Neurosci 16:869592. doi: 10.3389/fnins.2022.869592 PMID: 35844238
Objective: To investigate the effect of high-repetition/low-resistance tongue exercise on tongue function, strength, and structure.
Summary: The tongue plays a crucial role in swallowing and impairment can lead to dysphagia, particularly in motor neuron diseases such as amyotrophic lateral sclerosis. This study utilized the authors previously established inducible rodent model of dysphagia due to targeted degeneration of the hypoglossal-tongue axis by injecting cholera toxin B conjugated to saporin (CTB-SAP) into the genioglossus muscle of the tongue base for retrograde transport to the hypoglossal (XII) nucleus via the hypoglossal nerve, which provides the sole motor control of the tongue. Results showed that sham-exercised CTB-SAP rats had significant deficits in lick rate, swallow timing, and lick force. In exercised CTB-SAP rats, lick rate and lick force were preserved; however, swallow timing deficits persisted.
Usage: Rats received either a single “control” injection of unconjugated CTB + SAP (20μg CTB+25μg SAP) or CTB-SAP (Cat. #IT-14) injection (25μg of CTB conjugated to SAP) into the midline genioglossus muscle in the tongue base.
Related Products: CTB-SAP (Cat. #IT-14), Saporin (Cat. #PR-01)
Impact of limb phenotype on tongue denervation atrophy, dysphagia penetrance, and survival time in a mouse model of ALS
Mueller M, Thompson R, Osman KL, Andel E, DeJonge CA, Kington S, Stephenson Z, Hamad A, Bunyak F, Nichols NL, Lever TE (2022) Impact of limb phenotype on tongue denervation atrophy, dysphagia penetrance, and survival time in a mouse model of ALS. Dysphagia 37(6):1777-1795. doi: 10.1007/s00455-022-10442-4 PMID: 35426522
Related Products: CTB-SAP (Cat. #IT-14)
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