targeted-toxins

Boccia L, Le Foll C, Lutz TA (2020) Noradrenaline signaling in the LPBN mediates amylin’s and salmon calcitonin’s hypophagic effect in male rats. FASEB J 34(11):15448-15461. doi: 10.1096/fj.202001456RRR

Objective: To assess the phenotype of amylin activated LPBN (lateral parabrachial nucleus) neurons, especially to confirm the CGRPergic phenotype and to uncover the specific role of NA (noradrenaline) signaling from the AP to the LPBN.

Summary: The present study confirmed the central role of the LPBN in propagating amylin’s and sCT’s hypophagic action, and particularly the importance of AP → LPBN NA signaling in the mediation of this process, through the activation of LPBN (CGRP and non-CGRP) neurons.

Usage: The neuronal pathways used to process the physiological response to amylin were investigated using 50-ng injections of Anti-DBH-SAP (Cat. #IT-03) into the area postrema (AP) or 25 ng into the lateral parabrachial nucleus (Potes et al., 2010).

Related Products: Anti-DBH-SAP (Cat. #IT-03)

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.

See: Gulino R Neuroplasticity and Repair in Rodent Neurotoxic Models of Spinal Motoneuron Disease. Neural Plast 2016:2769735, 2016.

Related Products: CTB-SAP (Cat. #IT-14)

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.

See: Lind LA et al. 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, 2018.

Related Products: CTB-SAP (Cat. #IT-14)

Irvine KA, Sahbaie P, Ferguson AR, Clark JD (2020) Loss of diffuse noxious inhibitory control after traumatic brain injury in rats: A chronic issue. Exp Neurol 333:113428. doi: 10.1016/j.expneurol.2020.113428

Objective: To confirm hypothesis that dysfunctional descending noradrenergic and serotonergic pain control circuits may contribute to the loss of diffuse noxious inhibitory control (DNIC), a critical endogenous pain control mechanism, weeks to months after traumatic brain injury (TBI).

Summary: Results suggest that TBI causes maladaptation of descending nociceptive signaling mechanisms and changes in the function of both adrenergic and serotonergic circuits. Such changes could predispose those with TBI to chronic pain.

Usage: Anti-DBH-SAP (5 μg/5 μl) was injected in the left ventricle. Lesion of the LC resulted in failure of DNIC, an effect that mimics what is observed behaviorally after chronic TBI.

Related Products: Anti-DBH-SAP (Cat. #IT-03)

Ho IHT, Chan MTV, Wu WKK, Liu X (2020) Spinal microglia-neuron interactions in chronic pain. J Leukoc Biol 108:1575-1592. doi: 10.1002/JLB.3MR0520-695R

Summary: Spinal microglial activation is initiated shortly and persisted for more than 3 mo after partial sciatic nerve ligation. Intrathecal injection of Mac1-SAP, a saporin-conjugated anti-CD11b antibody to deplete microglia, abolished cold and mechanical allodynia for 2–12 wk after injury,92 supporting the role of activated microglia for chronic pain maintenance.

Related Products: Mac-1-SAP rat (Cat. #IT-33)

See Also:

• Echeverry S et al. Spinal microglia are required for long-term maintenance of neuropathic pain. Pain 158:1792-1801, 2017.

Tseng PY, Hoon MA (2020) Molecular genetics of kappa opioids in pain and itch sensations. Handb Exp Pharmacol . doi: 10.1007/164_2020_397

Summary: The authors review the functions of the kappa opioid receptor (KOR) and its endogenous agonists dynorphins in modulating itch and pain. Nppb-SAP ablation of neurons expressing the Natriuretic olypeptide B receptor greatly reduced itch responses evoked by histamine or by intrathecal administration of Nppb, suggesting that these neurons transmit itch signals from Nppb primary afferents.

See: Mishra SK et al. The cells and circuitry for itch responses in mice. Science 340(6135):968-971, 2013.

Related Products: Nppb-SAP (Cat. #IT-69)

Tapa S, Wang L, Francis Stuart SD, Wang Z, Jiang Y, Habecker BA, Ripplinger CM (2020) Adrenergic supersensitivity and impaired neural control of cardiac electrophysiology following regional cardiac sympathetic nerve loss. Sci Rep 10:18801. doi: 10.1038/s41598-020-75903-y

Summary: The authors present a novel mouse model of regional cardiac sympathetic hypo-innervation utilizing Anti-DBH-SAP.

Usage: Either 5μL of 40 ng/μL Anti-DBH-SAP or Mouse IgG-SAP (control) was applied three times directly to the exposed apical/anterior surface of the heart.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)

Guo J, Ba X, Matsuda M, Wei P, Jiang C, Sun W, Xiao L, Xiong D, Liao X, Hao Y (2020) Oxytocin elicits itch scratching behavior via spinal GRP/GRPR system. Front Neursci 14:581977. doi: 10.3389/fnins.2020.581977

Objective: To investigate the spinal mechanisms underlying oxytocin-induced scratching behavior and its relationship with the gastrin-releasing peptide (GRP)/GRP receptor (GRPR) pathway.

Summary: Intrathecal oxytocin triggered robust, transient scratching behavior in mice via spinal oxytocin receptors expressed on GRP neurons. Ablation of GRPR⁺ neurons with Bombesin-SAP significantly reduced scratching, demonstrating that the GRP/GRPR circuit mediates oxytocin-evoked itch signaling.

Usage: Bombesin-SAP (IT-40) was administered intrathecally at 400 ng in 10 µL sterile saline to selectively ablate spinal GRPR⁺ neurons two weeks before behavioral testing.

Related Products: Bombesin-SAP (Cat. #IT-40)

Dobryakova YV, Stepanichev MY, Markevich VA, Bolshakov AP (2020) Long-term potentiation in the hippocampal CA3 to CA1 synapses may be induced in vivo by activation of septal cholinergic inputs. Int J Neurosci 23:1-7. doi: 10.1080/00207454.2020.1822834

Objective: To clarify the role of septal input in the development of long-term potentiation (LTP) in this synapse.

Summary: Elimination of septal cholinergic neurons by 192-IgG-SAP abolished LTP development in both experimental series. This suppression of LTP in animals with a cholinergic deficit was not due to loss of hippocampal neurons.

Usage: Rats received intraseptal injections of 192-IgG-SAP (1.5 μg).

Related Products: 192-IgG-SAP (Cat. #IT-01)

Audira G, Ngoc Anh NT, Ngoc Hieu BT, Malhotra N, Siregar P, Villalobos O, Villaflores OB, Ger TR, Huang JC, Chen KH, Hsiao CD (2020) Evaluation of the adverse effects of chronic exposure to donepezil (an acetylcholinesterase inhibitor) in adult zebrafish by behavioral and biochemical assessments. Biomolecules 10(9):1340. doi: 10.3390/biom10091340 PMID: 32962160

Objective: The authors use zebrafish to conduct a deeper analysis of the potential adverse effects of DPZ on the short-term memory and behaviors of normal zebrafish by performing multiple behavioral and biochemical assays.

Summary: Chronic waterborne exposure to donepezil (DPZ) can severely induce adverse effects on normal zebrafish in a dose-dependent manner.

Related Products: 192-IgG-SAP (Cat. #IT-01)

See Also:

• Cutuli D et al. Neuroprotective effects of donepezil against cholinergic depletion. Alzheimers Res Ther 5(5):50, 2013.