targeted-toxins

Jeong D, Oh J, Lee J, Lee J, Cho Z, Chang J, Chang W (2016) Basal forebrain cholinergic deficits reduce glucose metabolism and function of cholinergic and gabaergic systems in the cingulate cortex. Yonsei Med J 57:165-172. doi: 10.3349/ymj.2016.57.1.165

Summary: A common result of cholinergic neuron loss in the hippocampus and cortical regions due to Alzheimer’s disease is a reduction in glucose metabolism. The authors examine the interaction between the cell loss and metabolic changes. Rats received 5-μg bilateral cortical injections of 192-IgG-SAP (Cat. #IT-01), were subject to water maze testing, and analyzed by 18F-2-fluoro-2-deoxyglucose positron emission tomography. Lesioned animals displayed decreased learning performance and reduced metabolic activity in the cingulate cortex.

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

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)

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)

Petrosini L, De Bartolo P, Cutuli D, Gelfo F (2016) Perinatal 192 IgG-saporin as neuroteratogen. Curr Top Behav Neurosci 29:111-123. doi: 10.1007/7854_2015_418

Summary: The authors discuss the effects of perinatal administration of 192-IgG-SAP (Cat. #IT-01) and areas of research that have been investigated through the use of these lesions. The chapter covers a description of 192-IgG-SAP, lesioning methods, and outlines the short- and long-term biochemical, structural, behavioral, and cognitive effects of 192-IgG-SAP administration.

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

Chen Y, Pan C, Xuan A, Xu L, Bao G, Liu F, Fang J, Long D (2015) Treatment efficacy of NGF nanoparticles combining neural stem cell transplantation on Alzheimer’s Disease model rats. Med Sci Monit 21:3608-3615. doi: 10.12659/msm.894567

Summary: NSC (neural stem cell) transplants into animals have been shown to compensate for the loss of cholinergic cells in the basal forebrain, a hallmark of Alzheimer’s disease. One hurdle to overcome is the actuation of NSC differentiation into the specific replacement cells needed. NGF has been shown to induce this differentiation, but it has a very short half-life and does not permeate tissue very effectively. In this work the authors administered 5 mcl of icv 192-IgG-SAP (Cat. #IT-01) to rats, followed by a graft of NCSs in the presence of NGF nanoparticles with a polymer coating. Rats receiving both NCSs and NGF nanoparticles showed significantly improved memory and learning functions as compared to control animals.

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

Li T, Yu Y, Cai H (2015) Effects of brain-derived neurotrophic factor-pretreated neuron stem cell transplantation on Alzheimer’s disease model mice. Int J Clin Exp Med 8:21947-21955.

Summary: In order to generate the AD mouse model, mu p75-SAP (1-1.2 μg/μL)  was injected to the bilateral icv areas.

Related Products: mu p75-SAP (Cat. #IT-16)

Helena C, Toporikova N, Kalil B, Stathopoulos A, Pogrebna V, Carolino R, Anselmo-Franci J, Bertram R (2015) KNDy neurons modulate the magnitude of the steroid-induced luteinizing hormone surges in ovariectomized rats. Endocrinology 156:4200-4213. doi: 10.1210/en.2015-1070

Summary: Maturation and reproductive function in mammals is controlled by the kisspeptin neuropeptide. Kisspeptin modulates numerous systems within this framework including the mediation of positive and negative feedback effects of estradiol on luteinizing hormone (LH). In the rat, two kisspeptin neuronal populations exist; one in the anteroventral periventricular nucleus (AVPV), and the KNDy (kisspeptin/ neurokinin B/dynorphin) neurons in the arcuate nucleus. In this work the authors examine the role of KNDy neurons in estradiol positive feedback effects by administering 10-ng bilateral injections of NK3-SAP (Cat. #IT-63) into the arcuate nucleus of rats. The results indicate that KNDy neurons use dynorphin to inhibit AVPV neurons, establishing a regulatory mechanism for the amplitude of steroid-induced LH surges.

Related Products: NKB-SAP (Cat. #IT-63)

Arora V, Morado-Urbina C, Aschenbrenner C, Hayashida K, Wang F, Martin T, Eisenach J, Peters C (2016) Disruption of spinal noradrenergic activation delays recovery of acute incision-induced hypersensitivity and increases spinal glial activation in the rat. J Pain 17:190-202. doi: 10.1016/j.jpain.2015.10.009

Summary: A significant percentage of patients who undergo surgery experience prolonged clinically impactful pain, reducing the quality of life and physical function. Disruption of the descending noradrenergic input has been hypothesized to be important to the generation of this type of pain state. Using an acute incision model, the authors administered 5 μg ofAnti-DBH-SAP (Cat. #IT-03) to the L5-L6 interspace of rats. Mouse IgG-SAP (Cat. #IT-18) was used as a control. Lesioned animals demonstrated a significant increase in mechanical hypersensitivity, and a smaller increase in thermal hypersensitivity. This and other results suggest that spinally projecting noradrenergic pathways are necessary for normal recovery from surgical incision, and possibly other types of pain.

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

Freiria-Oliveira A, Blanch G, Pedrino G, Cravo S, Murphy D, Menani J, Colombari D (2015) Catecholaminergic neurons in the comissural region of the nucleus of the solitary tract modulate hyperosmolality-induced responses. Am J Physiol Regul Integr Comp Physiol 309:R1082-1091. doi: 10.1152/ajpregu.00432.2014

Summary: Body fluid homeostasis and cardiovascular regulation are thought to be at least in part controlled by noradrenergic A2 neurons found in the nucleus of the solitary tract (NTS). In this work the authors investigated the involvement of A2 neurons of the commissural NTS in arterial pressure, as well as several body fluid homeostasis parameters. Rats received 12.6-ng injections of Anti-DBH-SAP (Cat. #IT-03) into the commissural NTS. Mouse IgG-SAP (Cat. #IT-18) was used as a control. Lesioned animals displayed increased c-Fos expression in the hypothalamic paraventricular nucleus when treated with hypertonic NaCl, and increased arterial pressure. The data indicate that commissural NTS A2 neurons are essential for inhibitory mechanisms that reduce water intake and pressor response to an acute increase in plasma osmolality.

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

Bourane S, Duan B, Koch S, Dalet A, Britz O, Garcia-Campmany L, Kim E, Cheng L, Ghosh A, Ma Q, Goulding M (2015) Gate control of mechanical itch by a subpopulation of spinal cord interneurons. Science 350:550-554. doi: 10.1126/science.aac8653

Summary: Light mechanical stimulation of the hairy skin can induce a form of itch known as mechanical itch. This itch sensation is normally suppressed by inputs from mechanoreceptors, however, in many forms of chronic itch, including alloknesis, this gating mechanism is lost. Scientists demonstrated that a population of spinal inhibitory interneurons (INs), that are defined by the expression of neuropeptide Y::Cre (NPY::Cre), act to gate mechanical itch. Mice in which dorsal NPY::Cre-derived neurons are selectively ablated or silenced develop mechanical itch without an increase in sensitivity to chemical itch or pain. This chronic itch state is histamine-independent and is transmitted independently of the GRP-GRPR signaling pathway. The scientists thereby revealed a dedicated spinal cord inhibitory pathway that gates the transmission of mechanical itch. Mice were given an intrathecal injection of 400 ng of Bombesin-SAP (Cat. #IT-40) in 10 ml of sterile saline to ablate GRPR-expressing neurons.

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