- Home
- Knowledge Base
- References
The establishment of a CSF-contacting nucleus “knockout” model animal.
Song SY, Zhang LC (2018) The establishment of a CSF-contacting nucleus “knockout” model animal. Front Neuroanat 12:22. doi: 10.3389/fnana.2018.00022
Objective: To establish a cerebrospinal fluid (CSF)-contacting nucleus-deficient model animal using cholera toxin B subunit-saporin (CTB-SAP).
Summary: The complete ablation occurred by Day 7 after CTB-SAP microinjection. A model animal that had no CSF-contacting nucleus was established after survival beyond that time point. No obvious effects were observed in the vital status of the model animals, and their survival was ensured. The common physiological parameters of model animals were stable. The present study provides a method to establish a CSF-contacting nucleus “knockout” model animal, which is similar to a gene knockout model animal for studying this particular nucleus in vivo.
Usage: 3 μl (500 ng) CTB-SAP was microinjected into the lateral ventricle.
Related Products: CTB-SAP (Cat. #IT-14)
Phrenic long-term facilitation following intrapleural CTB-SAP-induced respiratory motor neuron death.
Nichols NL, Craig TA, Tanner MA (2018) Phrenic long-term facilitation following intrapleural CTB-SAP-induced respiratory motor neuron death. Respir Physiol Neurobiol 256:43-49. doi: 10.1016/j.resp.2017.08.003
Objective: To study the impact of respiratory motor neuron death.
Summary: Intrapleural CTB-SAP mimics aspects of ALS. Seven days of CTB-SAP enhances respiratory plasticity.
Usage: Bilateral intrapleural injections of: 1) CTB-SAP (25 μg), or 2) unconjugated CTB and SAP (control).
Related Products: CTB-SAP (Cat. #IT-14), Saporin (Cat. #PR-01)
Adenosine 2A (A2A) receptor expression in rats with motor neuron death from intrapleural CTB-saporin injections
Craig TA, Brown SM, Nichols NL (2017) Adenosine 2A (A2A) receptor expression in rats with motor neuron death from intrapleural CTB-saporin injections. FASEB J 31(S1):873.14. Experimental Biology 2017 Meeting Abstracts. doi: 10.1096/fasebj.31.1_supplement.873.14
Related Products: CTB-SAP (Cat. #IT-14)
Phrenic long-term facilitation (pLTF) following acute intermittent hypoxia (AIH) is TrkB and PI3K/Akt dependent in rats with motor neuron death from intrapleural CTB-saporin injections
Nichols NL, Tanner M (2017) Phrenic long-term facilitation (pLTF) following acute intermittent hypoxia (AIH) is TrkB and PI3K/Akt dependent in rats with motor neuron death from intrapleural CTB-saporin injections. FASEB J 31(S1):1053.13. Experimental Biology 2017 Meeting Abstracts. doi: 10.1096/fasebj.31.1_supplement.1053.13
Related Products: CTB-SAP (Cat. #IT-14)
Sonic hedgehog and TDP-43 participate in the spontaneous locomotor recovery in a mouse model of spinal motoneuron disease
Gulino R, Parenti R, Gulisano M (2017) Sonic hedgehog and TDP-43 participate in the spontaneous locomotor recovery in a mouse model of spinal motoneuron disease. J Funct Morphol Kinesiol 2:11.. doi: 10.3390/jfmk2020011
Summary: The authors used a mouse model of neurotoxic motoneuron depletion to study the role of Sonic hedgehog and TDP-43 in the compensatory changes occurring after the lesion. The injection of cholera toxin-B saporin (CTB-SAP; Cat. #IT-14) into the gastrocnemius muscle caused a partial motoneuron death accompanied by an impairment of locomotion. Motor activity was significantly restored as soon as one month later.
Related Products: CTB-SAP (Cat. #IT-14)
Novel targets for modulation of plasticity in a mouse model of motoneuron degeneration.
Gulino R, Forte S, Parenti R, Gulisano M (2016) Novel targets for modulation of plasticity in a mouse model of motoneuron degeneration. Neuroscience 2016 Abstracts 812.14 / OO13. Society for Neuroscience, San Diego, CA.
Summary: A successful spinal cord repairing strategy should involve the activation of neural precursor cells. Unfortunately, their ability to generate neurons aſter injury appears limited. Another process promoting functional recovery is synaptic plasticity. We have previously studied some mechanisms of spinal plasticity by using a mouse model of motoneuron depletion induced by cholera toxin-B saporin. TDP-43 is a nuclear RNA/DNA binding protein involved in amyotrophic lateral sclerosis. Although considerable attention has been devoted to the toxic effects of the TDP-43 cytoplasmic aggregates, the functional role of this factor remains poorly investigated. Notably, TDP-43 is present in the dendrites where it behaves as a modulator of local RNA translation. Moreover, it is crucial for synaptic plasticity and locomotion in Drosophila. Here, we would like to deepen the investigation of this model of spinal plasticity. Aſter lesion, we observed a glial reaction and an activity-dependent modification of Synapsin-I, Shh, Noggin, Numb and TDP-43 proteins. Multivariate regression was used to model the possible association between these proteins, as well as with the motor performance. We found that Shh and Noggin could affect motor performance and that these proteins could be associated with both TDP-43 and Numb, thus suggesting that TDP-43 is likely an important regulator of synaptic plasticity. Given the well-known role of morphogens such as Shh, Noggin and Numb in neurogenesis and the above described functions of TDP-43, we believe that an in vivo manipulation of their signaling pathways after lesion could represent a putative method of improving regeneration and recovery by affecting synaptic plasticity and/or neurogenesis.
Related Products: CTB-SAP (Cat. #IT-14)
Neuroprotective effects of testosterone metabolites and dependency on receptor action on the morphology of somatic motoneurons following the death of neighboring motoneurons.
Cai Y, Chew C, Muñoz F, Sengelaub D (2017) Neuroprotective effects of testosterone metabolites and dependency on receptor action on the morphology of somatic motoneurons following the death of neighboring motoneurons. Dev Neurobiol 77:691-707.. doi: 10.1002/dneu.22445
Summary: In this study the authors examined whether the protective effects of testosterone could be mediated via its androgenic or estrogenic metabolites and if these neuroprotective effects were mediated through steroid hormone receptors. Analysis was done using receptor antagonists to attempt to prevent the neuroprotective effects of hormones after partial motoneuron depletion. These motoneurons were selectively killed by intramuscular injection of CTB-SAP (2 ul, 0.1%) (Cat. #IT-14). Compared with intact normal animals, partial motoneuron depletion resulted in decreased dendritic length in remaining quadriceps motoneurons. Dendritic atrophy was attenuated with both dihydrotestosterone and estradiol treatment to a degree similar to that seen with testosterone and attenuation of atrophy was prevented by receptor blockade. Together, the results suggest that neuroprotective effects on motoneurons can be mediated by either androgenic or estrogenic hormones and require action via steroid hormone receptors, further supporting a role for hormones as neurotherapeutic agents in the injured nervous system.
Related Products: CTB-SAP (Cat. #IT-14)
Role of the RVM in descending pain regulation originating from the cerebrospinal fluid-contacting nucleus.
Fei Y, Wang X, Chen S, Zhou Q, Zhang C, Li Y, Sun L, Zhang L (2016) Role of the RVM in descending pain regulation originating from the cerebrospinal fluid-contacting nucleus. Neurochem Res 41:1651-1661. doi: 10.1007/s11064-016-1880-6
Summary: The researchers investigated whether the CSF-contacting nucleus contributed to descending pain modulation in normal and neuropathic rats, and detected the 5-HT expression changes in both RVM and spinal dorsal cord. They also detected the possible anatomical and function correlation between the CSF-contacting nucleus and the RVM. Targeted ablation of the CSF-contacting nucleus was performed using CTB-SAP (Cat. #IT-14; 500 ng/3 μl), which was administered i.c.v. to the normal rats and rats 7 days before the CCI procedure. Based on the findings of the present study, they believe that the CSF-contacting nucleus may act as a component of descending pain regulation system. RVM, which acts as an important brain nucleus, is involved in the relay of nociceptive information between the CSF-contacting nucleus and spinal cord. Moreover, RVM 5-HT system plays a critical role in descending pain inhibition originating from the CSF-contacting nucleus.
Related Products: CTB-SAP (Cat. #IT-14)
Neuroplasticity and repair in rodent neurotoxic models of spinal motoneuron disease.
Gulino R (2016) Neuroplasticity and repair in rodent neurotoxic models of spinal motoneuron disease. Neural Plast 2016:2769735. doi: 10.1155/2016/2769735
Summary: TDP-43 (Transactive response DNA-binding protein) is a highly conserved nuclear protein that binds both DNA and RNA. It has been found in cytoplasmic protein aggregates of patients with conditions such as amyotrophic lateral sclerosis and Alzheimer’s disease. In this work the authors examine the role of TDP-43 in spinal cord plasticity. Mice received bilateral 3-μg injections of CTB-SAP (Cat. #IT-14) into the lateral and medial gastrocnemius muscles. The results indicate that motor performance is dependent on expression of synapsin-I, which in turn may be dependent on TDP-43.
Related Products: CTB-SAP (Cat. #IT-14)
Targeted ablation of cardiac sympathetic neurons: A promising approach to prevent sudden cardiac death.
Xia W, Liu Y (2016) Targeted ablation of cardiac sympathetic neurons: A promising approach to prevent sudden cardiac death. Int J Cardiol 202:425-426. doi: 10.1016/j.ijcard.2015.09.049
Summary: Sudden cardiac death (SCD) refers to an unexpected death due to cardiovascular causes, occurring generally within 1 hr of symptom onset, in a person without any prior condition that would appear fatal. Currently, the implantable cardioverter-defibrillator (ICD) has been shown to be the most effective therapy for preventing SCD. However, the occurrence of lead complications is significant and more importantly, the ICD implantation remains costly and the quality of life for recipients is significantly affected with appropriate and inappropriate shocks. Sympathetic activation plays an important role in the pathophysiology of arrhythmias leading to SCD, and neuraxial modulation is emerging as an important avenue of therapeutic intervention. The authors demonstrate that targeted ablation of cardiac sympathetic neurons by bilateral stellate ganglia injection of CTB-SAP (Cat. #IT-14) is a novel method for sympathetic blockade. CTB-SAP will be retrogradely transported to the plasma membranse of sympathetic preganglionic neurons (SPNs) and bind to the GM1 gangliosides and subsequently ablate these neurons. Targeted ablation of cardiac sympathetic neurons by injection of CTB-SAP avoids the limitations of medical therapy and thoracic sympathectomy, such as incomplete compliance, Horner’s syndrome, and compensatory hyperhidrosis. Furthermore, they found that targeted ablation of cardiac sympathetic neurons reduces resting, reflex and exercise-induced sustained ventricular tachycardia, associated with a reduced number of neurons in the stellate ganglia and spinal cord, as well as a reduced left ventricular norepinephrine content and sympathetic innervation density. Therefore, targeted ablation of cardiac sympathetic neurons may be a promising approach to prevent SCD via regulating the cardiac autonomic nervous system.
Related Products: CTB-SAP (Cat. #IT-14)