References

Takeuchi Y, Nagy AJ, Barcsai L, Li Q, Ohsawa M, Mizuseki K, Berényi A (2021) The medial septum as a potential target for treating brain disorders associated with oscillopathies. Front Neural Circuits 15:701080. doi: 10.3389/fncir.2021.701080

Summary: The medial septum (MS) may be a potential target for treating neurological and psychiatric disorders with abnormal oscillations (oscillopathies) to restore healthy patterns or erase undesired ones. The time-targeted strategy for the MS stimulation may provide an effective way of treating multiple disorders.

Usage: 192-IgG-SAP. The MS cholinergic neurons along with theta oscillations are known to be essential for memory because selective lesion of the cholinergic neurons resulted in spatial memory impairments (150 ng; Easton et al., 2011) (5.04 μg icv; Jeong et al., 2014). Orexin-SAP. The enhanced gamma oscillations and altered PPI and auditory gating created by psychoactive drugs in rats were mediated by GABAergic neurons in the MS because they were abolished by ablation of these neurons by Orexin-SAP (140 ng total bilateral; Ma et al., 2012). mu p75-SAP. Anxious environment-induced type 2 theta oscillation and associated anxiety were shown to be dependent on the MS cholinergic neurons because lesion of MS cholinergic neurons reduced them (0.65 or 1.3 µg, bilateral; Nag et al., 2009).

Related Products: 192-IgG-SAP (Cat. #IT-01), mu p75-SAP (Cat. #IT-16), Orexin-B-SAP (Cat. #IT-20)

See Also:

• Easton A et al. Medial septal cholinergic neurons are necessary for context-place memory but not episodic-like memory. Hippocampus 21(9):1021-1027, 2011.
• Jeong D et al. Improvements in memory after medial septum stimulation are associated with changes in hippocampal cholinergic activity and neurogenesis. Biomed Res Int 2014:568587, 2014.
• Ma J et al. Septohippocampal GABAergic neurons mediate the altered behaviors induced by n-methyl-D-aspartate receptor antagonists. Hippocampus 22(12):2208-2218, 2012.
• Nag N et al. Efficacy of a murine-p75-saporin immunotoxin for selective lesions of basal forebrain cholinergic neurons in mice. Neurosci Lett 452:247-251, 2009.

Kucinski A, Sarter M (2021) Reduction of falls in a rat model of PD falls by the M1 PAM TAK-071. Psychopharmacology (Berl) 238(7):1953-1964. doi: 10.1007/s00213-021-05822-x

Summary: In addition to the disease-defining motor symptoms, patients with Parkinson’s disease (PD) exhibit gait dysfunction, postural instability, and a propensity for falls. The muscarinic M1-positive allosteric modulator (PAM) TAK-071 improves the attentional performance of rats with BF cholinergic losses. The authors previously developed a rodent model of PD falls by demonstrating that rats with dual basal forebrain cholinergic and mediodorsal striatal dopamine losses (“DL rats”) exhibit a heightened fall rate when required to traverse dynamic surfaces. This study tested the hypothesis that TAK-071 reduces fall rates in DL rats.

Usage: Rats received bilateral infusions of 192-IgG-SAP (200 ng/μL; 0.8 μL/hemisphere) or an equal volume of artificial cerebral spinal fluid into the nucleus basalis and substantia innominata of the basal forebrain.

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

Li Y, Bao Y, Zheng H, Qin Y, Hua B (2021) Can Src protein tyrosine kinase inhibitors be combined with opioid analgesics? Src and opioid-induced tolerance, hyperalgesia and addiction. Biomed Pharmacother 139:111653. doi: 10.1016/j.biopha.2021.111653

Summary: In this review the authors discuss the important role Src protein tyrosine kinase plays in the adverse consequences of clinical application of opioids

Usage: Intrathecal injection of Mac-1-SAP depletes microglial cells in the spinal dorsal horn and alleviates the loss of anti-nociception of morphine and prevents the decrease in morphine potency. This demonstrates that spinal microglial cells are necessary for morphine tolerance (15 µg; Leduc-Pessah et al., 2017).

See: Leduc-Pessah H et al. Site-Specific Regulation of P2X7 Receptor Function in Microglia Gates Morphine Analgesic Tolerance. J Neurosci 37:10154-10172, 2017.

Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)

Zhu L, Liu Z, Huang LP, Zhou HR, Cao Y, Yang XP, Wang BJ, Yang ZL, Chen J (2021) Angiotensin (1-7) alleviates postresuscitation myocardial dysfunction by suppressing oxidative stress through the phosphoinositide 3-kinase, protein kinase b, and endothelial nitric oxide synthase signaling pathway. J Cardiovasc Pharmacol 78(1):e65-e76. doi: 10.1097/fjc.0000000000001037 PMID: 33929390

Objective: To investigate the role of the Ang (1-7)-MasR axis in postresuscitation myocardial dysfunction (PRMD) and its associated mechanism.

Summary: The Ang (1-7)-MasR axis can alleviate PRMD by reducing myocardial tissue damage and oxidative stress through activation of the phosphoinositide 3-kinase-protein kinase B-endothelial nitric oxide synthase signaling pathway and provide a new direction for the clinical treatment of PRMD.

Usage: Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified

Related Products: Angiotensin II receptor (AT-1R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N27AP)

Gross C (2021) PARVing the way to cap translation for seizure control. Epilepsy Curr 21(5):360-362. doi: 10.1177/15357597211027010

Summary: Loss of GABAergic interneurons leads to spontaneous recurrent seizures that persist over months if the amount and spatial spread of initial inhibitory neuron loss is sufficient.

Usage: Intrahippocampal injections of SSP-SAP (0.4 ng/10 nL) were performed using a 0.5-μL Neuros Syringe lowered into four hippocampal sites along both the transverse and longitudinal hippocampal axes bilaterally.

See: Chun E et al. Targeted hippocampal GABA neuron ablation by Stable Substance P-saporin causes hippocampal sclerosis and chronic epilepsy in rats. Epilepsia 60(5):e52-e57, 2019.

Related Products: SSP-SAP (Cat. #IT-11)

Middleton SJ, Barry AM, Comini M, Li Y, Ray PR, Shiers S, Themistocleous AC, Uhelski ML, Yang X, Dougherty PM, Price TJ, Bennett DL (2021) Studying human nociceptors: from fundamentals to clinic. Brain 144(5):1312-1335. doi: 10.1093/brain/awab048

Summary: The authors injected 5 µg of IB4-SAP into the sciatic nerve in the left thigh. Lesioned animals displayed attenuated NGF-induced hyperalgesia, as well as differences in other pain-model markers.

See: Tarpley JW et al. The behavioral and neuroanatomical effects of IB(4)-saporin treatment in rat models of nociceptive and neuropathic pain. Brain Res 1029(1):65-76, 2004.

Related Products: IB4-SAP (Cat. #IT-10)

Petrosini L, De Bartolo P, Cutuli D (2021) Neurotoxic effects, mechanisms, and outcome of 192 IgG-Saporin lesions. RM Kostrzewa (Ed.): Handbook of Neurotoxicity . Springer, Cham doi: 10.1007/978-3-030-71519-9_79-1

Summary: 192-IgG-saporin selectively destroys basal forebrain cholinergic neurons that provide cholinergic input to the hippocampus, entire cortical mantle, amygdala, and olfactory bulb. Immunotoxic lesions by 192-IgG-saporin represent a valid animal model of Alzheimer’s disease, given the degeneration of basal cholinergic system present in this pathology. The selective lesioning of cholinergic innervation by means of 192-IgG-saporin (injected i.p. or i.c.v.) is able to interfere with experience-dependent plasticity.

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

Gavini MP, Mahmood A, Belenchia AM, Beauparlant P, Kumar SA, Ardhanari S, DeMarco VG, Pulakat L (2021) Suppression of inflammatory cardiac cytokine network in rats with untreated obesity and pre-diabetes by AT2 receptor agonist NP-6A4. Front Pharmacol 12:693167. doi: 10.3389/fphar.2021.693167 PMID: 34220518

Objective: To determine whether NP-6A4 (a new AT2R peptide agonist with an FDA orphan drug designation for pediatric cardiomyopathy) would mitigate cardiac damage from chronic inflammation induced by untreated obesity.

Summary: Seventeen pro-inflammatory and pro-fibrotic cytokines that increase during lethal cytokine storms caused by infections such as COVID-19 were among the cytokines suppressed by NP-6A4 treatment in ZO rat heart. Thus, NP-6A4 activates a novel anti-inflammatory network comprised of 21 proteins in the heart that was not reported previously. Since NP-6A4’s unique mode of action suppresses pro-inflammatory cytokine network and attenuates myocardial damage, it can be an ideal adjuvant drug with other anti-glycemic, anti-hypertensive, standard-of-care drugs to protect the heart tissues from pro-inflammatory and pro-fibrotic cytokine attack induced by obesity.

Usage: Immunohistochemistry, 5-micrometer heart sections

Related Products: Angiotensin II receptor (AT-2R) Rabbit Polyclonal, affinity-purified (Cat. #AB-N28AP)

Vicario N, Spitale FM, Tibullo D, Giallongo C, Amorini AM, Scandura G, Spoto G, Saab MW, D’Aprile S, Alberghina C, Mangione R, Bernstock JD, Botta C, Gulisano M, Buratti E, Leanza G, Zorec R, Vecchio M, Di Rosa M, Li Volti G, Lazzarino G, Parenti R, Gulino R (2021) Clobetasol promotes neuromuscular plasticity in mice after motoneuronal loss via sonic hedgehog signaling, immunomodulation and metabolic rebalancing. Cell Death Dis 12(7):625. doi: 10.1038/s41419-021-03907-1

Summary: The focal removal of confined populations of spinal MNs by injection of CTB-SAP has proven to be useful in mimicking respiratory dysfunction, dysphagia, and focal MN loss.

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

See Also:

• Lind LA et al. Tongue and hypoglossal morphology after intralingual cholera toxin B-saporin injection. Muscle Nerve 63(3):413-420, 2021.
• Gulino R et al. Neuromuscular plasticity in a mouse neurotoxic model of spinal motoneuronal loss. Int J Mol Sci 20(6):1500, 2019.
• Nichols N et al. Respiratory function after selective respiratory motor neuron death from intrapleural CTB-saporin injections. Exp Neurol 267:18-29, 2015.
• Gulino R et al. Expression of cell fate determinants and plastic changes after neurotoxic lesion of adult mice spinal cord by cholera toxin-B saporin. Eur J Neurosci 31(8):1423-1434, 2010.

Llorente-Ovejero A, Martínez-Gardeazabal J, Moreno-Rodríguez M, Lombardero L, González de San Román E, Manuel I, Giralt MT, Rodríguez-Puertas R (2021) Specific phospholipid modulation by muscarinic signaling in a rat lesion model of Alzheimer’s disease. ACS Chem Neurosci 12(12):2167-2181. doi: 10.1021/acschemneuro.1c00169 PMID: 34037379

Objective: To evaluate the lipid composition and muscarinic signaling in brain areas related to cognitive processes.

Summary: Using a rat model of BFCN lesion, this study evaluated the lipid composition and muscarinic signaling in brain areas related to cognitive processes. Results suggest that the modulation of specific lipid metabolic routes could represent an alternative therapeutic strategy to potentiate cholinergic neurotransmission and preserve cell membrane integrity in AD.

Usage: 192-IgG-SAP was dissolved in aCSF under aseptic conditions to a final concentration of 130 ng/ml. aCSF or 192-IgG-SAP was bilaterally injected (1 ml/hemisphere) at a constant rate of 0.2 ml/min. to selectively eliminate BFCN in the NBM.

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

See Also:

• Llorente-ovejero A et al. Increase in cortical endocannabinoid signaling in a rat model of basal forebrain cholinergic dysfunction. Neuroscience 362:206-218, 2017.