References

Toledo C, Del Rio R (2024) Cardiorespiratory disturbances in Alzheimer’s disease: A focus on the contribution of sympathetic premotor neurons. Am Physiol Summit 39(S1) doi: 10.1152/physiol.2024.39.S1.2540

Objective: To characterize cardiorespiratory function in AD patients and then to determine the role of RVLM-C1 neurons in autonomic and sleep-disordered breathing in APP/PS1 double transgenic mice, and experimental model showing AD-like pathology.

Summary: Results show that RVLM-C1 neurons play a main role in the development/maintenance of cardiorespiratory disorders in experimental AD.

Usage: Bilateral stereotaxic injections of Anti-DBH-SAP (IT-03) into the RVLM were used to selectively destroy C1 neurons.

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

Bohl JM, Hassan AR, Sharpe ZJ, Kola M, Ayub M, Pandey Y, Shehu A, Ichinose T (2024) Melanopsin ganglion cells in the mouse retina independently evoke pupillary light reflex. bioRxiv doi: 10.1101/2024.05.14.594181

Objective: To examine the role of rod and cone photoreceptors in pupillary light reflex (PLR) by acutely ablating photoreceptors.

Summary: Results demonstrate that ipRGCs are the major contributor to the PLR induced by high light.

Usage: Immunohistochemistry (AB-N39) (1:5000).

Related Products: Melanopsin Rabbit Polyclonal, affinity-purified (Cat. #AB-N39)

Contreras E, Liang C, Mahoney HL, Javier JL, Luce ML, Labastida Medina K, Bozza T, Schmidt TM (2024) Flp-recombinase mouse line for genetic manipulation of ipRGCs. bioRxiv doi: 10.1101/2024.05.06.592761 PMID: 38766000

Objective: To report the generation and characterization of a new mouse line (Opn4FlpO), in which FlpO is expressed from the Opn4 locus, to manipulate the melanopsin-expressing, intrinsically photosensitive retinal ganglion cells.

Summary: The Opn4FlpO mouse line drives Flp-recombinase expression specifically within ipRGCs, with robust recombination in M1-M3 ipRGC subtypes. This model is a valuable tool for investigating these retinal cells’ physiological and behavioral roles.

Usage: Retinal histology (1:2000 dilution) (AB-N38).

Related Products: Melanopsin Rabbit Polyclonal (Cat. #AB-N38)

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)

Shivakumar AB, Mehak SF, Jijimon F, Gangadharan G (2024) Extra-hippocampal contributions to social memory: The role of septal nuclei. Biol Psychiatry 6:835-847. doi: 10.1016/j.biopsych.2024.04.018 PMID: 38718881

Objective: Review neural circuit mechanisms that underlie social memory, with a special emphasis on the septum.

Summary: Understanding the complexities of the septohippocampal axis will allow targeted therapies to be developed to improve social memory deficits and enhance overall cognitive function.

Usage: Medial septum lesions in rats with 192-IgG-SAP (IT-01).

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

See Also:

• Vale-Martinez A et al. Selective lesions of basal forebrain cholinergic neurons produce anterograde and retrograde deficits in a social transmission of food preference task in rats. Eur J Neurosci 16(6):983-998, 2002.
• Berger-Sweeney J, Stearns NA, Frick KM, Beard B, Baxter MG (2000) Cholinergic basal forebrain is critical for social transmission of food preferences. Hippocampus 10(6):729-738. doi: 10.1002/1098-1063(2000)10:6<729::AID-HIPO1010>3.0.CO;2-M PMID: 11153718

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)

Pandala N, Han I, Meyering E, Stone EM, Mullins RF, Tucker BA (2024) iPSC derived choroidal endothelial cell delivery using laminin-based hydrogels for the treatment of AMD. ARVO Annual Meeting 65(7):1542.

Objective: To demonstrate an interventional therapy for age-related macular degeneration (AMD) using a rat model.

Summary: In this study, induced pluripotent stem cells (iPSCs) were injected into the eyes of rats that had undergone Anti-CD105-SAP-induced choroidal cell death, mimicking the pathology of AMD. The efficacy of the iPSC treatment was evaluated by comparing donor cell survival, retention, and integration in treated eyes versus controls that did not receive iPSCs.

Usage: Anti-CD105-SAP (IT-80) was administered via supra-choroidal injection at a concentration of 0.05 mg/ml to selectively induce choroidal endothelial cell death.

Related Products: Anti-CD105-SAP (Cat. #IT-80)

Han I, Pandala N, Haefeli L, Lang MJ, Stone EM, Mullins RF, Tucker BA (2024) Development of chemically induced choroidal injury models for the study and treatment of AMD. ARVO Annual Meeting 65(7):5382.

Objective: To describe the development of Age-Related Macular Degeneration (AMD) models through the targeted injury of choroidal cells in the eye.

Summary: Anti-CD38-SAP (BETA-016) and Anti-CD105-SAP (IT-80) were utilized to selectively lesion choroidal cells in the eyes of mice, creating an AMD model. Both agents demonstrated localized effects with no observed systemic toxicity at the administered doses, contrasting with the broader toxicity seen with Sodium Iodate, another lesioning agent examined.

Usage: Different doses of Anti-CD38-SAP and Anti-CD105-SAP (0.05, 0.25, and 0.5 mg/ml; 10 μL/eye) were injected suprachoroidally into the eyes of mice to induce the desired choroidal cell lesions.

Related Products: Anti-CD105-SAP (Cat. #IT-80)

Matsuda T, Morigaki R, Hayasawa H, Koyama H, Oda T, Miyake K, Takagi Y (2024) Striatal parvalbumin interneurons are activated in a mouse model of cerebellar dystonia. Dis Model Mech 17(5):dmm050338. doi: 10.1242/dmm.050338 PMID: 38616770

Objective: To examine the influence of cerebellar abnormalities on the basal ganglia circuitry to investigate dystonia pathophysiology.

Summary: Dystonia is a disorder characterized by twisting, repetitive movements, and abnormal postures induced by sustained muscle contractions. This study utilized a cerebellar dystonia mouse model to examine the cerebellum’s contribution. The authors found that modulating parvalbumin (PV) interneurons might provide a novel treatment strategy.

Usage: In order to selectively ablate dorsolateral striatal PV interneurons, Streptavidin-ZAP (Cat. #IT-27) was mixed equimolar with biotinylated anti-PV and diluted with PBS by 1:100 and 3 ul injected into the striatum of mice. BIgG-SAP Rabbit (Cat. #IT-75) was used as the control.

Related Products: Streptavidin-ZAP (Cat. #IT-27), BIgG-SAP Rabbit (Cat. #IT-75)

Masmudi-Martín M, Navarro-Lobato I, López-Aranda MF, Quiros-Ortega ME, Carretero-Rey M, Garcia-Garrido MF, López Téllez JF, Jiménez-Recuerda I, Muñoz de Leon López CA, Khan ZU (2024) Brain areas interconnected to ventral pathway circuits are independently able to induce enhancement in object recognition memory and cause reversal in object recognition memory deficit. CNS Neurosci Ther 30(4):e14727. doi: 10.1111/cns.14727 PMID: 38644593

Objective: Use OX7-SAP to create an object-recognition memory deficit model in rats.

Summary: Ventral pathway circuits are responsible for part of object recognition memory. Lesioning with OX7-SAP, a way to selectively remove CD90-expressing neuronal cells, can create a knockout model of object recognition memory, and lesioning in specific parts of the brain can construct a map of object recognition memory function.

Usage: Rats were lesioned with OX7-SAP in either the brain’s perirhinal cortex, frontal cortex, or Area V2 and assessed for object recognition memory deficits. (0.2μg in 1μL, IT-02)

Related Products: OX7-SAP (Cat. #IT-02)