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Rescuing the attentional performance of rats with cholinergic losses by the M1 positive allosteric modulator TAK-071
Kucinski A, Phillips KB, Koshy Cherian A, Sarter M (2020) Rescuing the attentional performance of rats with cholinergic losses by the M1 positive allosteric modulator TAK-071. Psychopharmacology (Berl) 237(1):137-153. doi: 10.1007/s00213-019-05354-5 PMID: 31620809
Related Products: 192-IgG-SAP (Cat. #IT-01)
Astroglia in Alzheimer’s Disease.
Verkhratsky A, Parpura V, Rodriguez-Arellano J, Zorec R (2019) Astroglia in Alzheimer’s Disease. (eds. Verkhratsky A, Ho M, Zorec R, Parpura V). In: Advances in Experimental Medicine and Biology: Neuroglia in Neurodegenerative Diseases. 1175:273-324. Springer, Singapore. doi: 10.1007/978-981-13-9913-8_11
Summary: A review of the tools for creating animal models of Alzheimer’s Disease. 192-IgG-SAP binds selectively and irreversibly to low-affinity nerve growth factor receptor interrupting cholinergic neuronal protein synthesis was employed. Anti-DBH-SAP binds dopamine-β-hydroxylase, which is not only localized mainly in the cytosol, but also at the plasma membrane surface of noradrenergic neurons. Anti-DBH-SAP produced specific and dose-dependent depletions of locus coeruleus neurons, with no effects on other cholinergic, dopaminergic or serotonergic neuronal populations. The possibility to induce a partial or total noradrenergic loss (by varying the injected dose) makes this immunotoxic approach an ideal model to study events within the noradrenergic projection system, as they occur during age-related demise of locus coeruleus in humans.
Related Products: 192-IgG-SAP (Cat. #IT-01), Anti-DBH-SAP (Cat. #IT-03)
Micro- and macro-psychological analyses of attention and the role of cholinergic systems
Phillips K (2019) Micro- and macro-psychological analyses of attention and the role of cholinergic systems. University of Michigan Thesis. doi: 2027.42/151673
Objective: To determine the validity of behavioral tasks used to reveal neurobehavioral and neurocognitive mechanisms of attention.
Summary: The opposing cognitive-motivational styles of sign-trackers and goal-trackers, while originating in different approaches to food and drug cues, provide us with a crucial insight into the individual differences and specific vulnerabilities for attentional processing and performance.
Usage: Bilateral bolus infusions of 192-IgG-SAP (0.8 μl/hemisphere).
Related Products: 192-IgG-SAP (Cat. #IT-01)
Are some animal models more equal than others? A case study on the translational value of animal models of efficacy for Alzheimer’s disease.
Veening-Griffioen DH, Ferreira GS, van Meer PJK, Boon WPC, Gispen-de Wied CC, Moors EHM, Schellekens H (2019) Are some animal models more equal than others? A case study on the translational value of animal models of efficacy for Alzheimer’s disease. Eur J Pharmacol 859:172524. doi: 10.1016/j.ejphar.2019.172524 PMID: 31291566
Related Products: 192-IgG-SAP (Cat. #IT-01)
Partial depletion of septohippocampal cholinergic cells reduces seizure susceptibility, but does not mitigate hippocampal neurodegeneration in the kainate model of epilepsy.
Soares JI, Da Costa C, Ferreira MH, Andrade PA, Maia GH, Lukoyanov NV (2019) Partial depletion of septohippocampal cholinergic cells reduces seizure susceptibility, but does not mitigate hippocampal neurodegeneration in the kainate model of epilepsy. Brain Res 1717:235-246. doi: 10.1016/j.brainres.2019.04.027
Objective: To examine how the inhibition of epilepsy-related cholinergic plasticity may be reflected in seizure susceptibility and/or in the development of chronic epilepsy and its neurological consequences.
Summary: These data suggest that seizure-induced plasticity of cholinergic cells may indeed enhance seizure susceptibility and contribute to epileptogenic processes. They do not support the hypothesis that epilepsy-related hypertrophy of cholinergic neurons may potentiate hippocampal cell loss and respective behavioral impairments.
Usage: Bilateral lesions of cholinergic cells were made by infusing 0.5 μl of 192-IgG-saporin (0.08 μg/μl saline solution) into the hippocampus.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Cholinergic deficit induced by central administration of 192IgG-Saporin is associated with activation of microglia and cell loss in the dorsal hippocampus of rats
Dobryakova YV, Volobueva MN, Manolova AO, Medvedeva TM, Kvichansky AA, Gulyaeva NV, Markevich VA, Stepanichev MY, Bolshakov AP (2019) Cholinergic deficit induced by central administration of 192IgG-Saporin is associated with activation of microglia and cell loss in the dorsal hippocampus of rats. Front Neurosci 13:146. doi: 10.3389/fnins.2019.00146
Objective: To study the histopathology of the hippocampus and the responses of microglia and astrocytes using immunohistochemistry and neuroglial gene expression.
Summary: Cholinergic degeneration in the medial septal area induced by intracerebroventricular administration of 192IgG-saporin results in an increase in the number of microglial cells and neuron degeneration in the dorsal hippocampus.
Usage: 192-IgG-SAP was injected bilaterally into both ventricles (i.c.v.) at a dose of 4 μg/site.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Basal forebrain chemogenetic inhibition disrupts the superior complex movement control of goal-tracking rats.
Kucinski A, Kim Y, Sarter M (2019) Basal forebrain chemogenetic inhibition disrupts the superior complex movement control of goal-tracking rats. Behav Neurosci 133:121-134. doi: 10.1037/bne0000290
Usage: Basal forebrain cholinergic neurons situated in the nucleus basalis and substantia innominata were targeted with 192-IgG-SAP in aCSF infused bilaterally (200 ng/μL; 0.8 μL/hemisphere).
Related Products: 192-IgG-SAP (Cat. #IT-01)
Co-treatment with rivastigmine and idalopirdine reduces the propensity for falls in a rat model of falls in Parkinson’s disease.
Koshy Cherian A, Kucinski A, Wu R, deJong IEM, Sarter M (2019) Co-treatment with rivastigmine and idalopirdine reduces the propensity for falls in a rat model of falls in Parkinson’s disease. Psychopharmacology 236:1701–1715. doi: 10.1007/s00213-018-5150-y
Objective: The authors used a longer and more taxing rotating beam apparatus to determine the potential therapeutic efficacy of idalopirdine when combined with rivastigmine.
Summary: The results extend the prediction that the combined treatment with idalopirdine and an AChE inhibitor improves complex movement control and reduces propensity for falls in patients with movement disorders.
Usage: Basal forebrain cholinergic neurons situated in the nucleus basalis and substantia innominata were targeted with 192-IgG-SAP in aCSF infused bilaterally (200 ng/μL; 0.8 μL/hemisphere).
Related Products: 192-IgG-SAP (Cat. #IT-01)
Cholinergic input to the hippocampus is not required for a model of episodic memory in the rat, even with multiple consecutive events.
Seel S, Eacott M, Langston R, Easton A (2018) Cholinergic input to the hippocampus is not required for a model of episodic memory in the rat, even with multiple consecutive events. Behav Brain Res 354:48-54. doi: 10.1016/j.bbr.2017.06.001
Summary: The authors use 192-IgG-SAP (Cat. #IT-01) to examine episodic memory. Continual trials versions of an episodic memory task are unimpaired by cholinergic lesions of the medial septum. In contrast continual trial versions of a location-context (where-which) task are impaired in the same animals. The results replicate the effects of lesions on one-trial a day versions of the same tasks. Increasing the amount of interference between trials by increasing the overlap of features in consecutive events has no effect on the behavioural outcome of these lesions. The result is interpreted in light of models of acetylcholine function centered around pattern separation.
Related Products: 192-IgG-SAP (Cat. #IT-01)
Learning and memory improvement mediated by CB1 cannabinoid receptors in animal models of cholinergic dysfunction
Moreno-Rodriguez M, Martinez-Gardeazabal J, Llorente-Ovejero A, Lombardero L, Manuel I, Rodriguez-Puertas R (2018) Learning and memory improvement mediated by CB1 cannabinoid receptors in animal models of cholinergic dysfunction. Neuroscience 2018 Abstracts 049.05 / S3. Society for Neuroscience, San Diego, CA.
Summary: The selective vulnerability of the basal forebrain cholinergic system (BFCS) is responsible for most of the clinical alterations in learning and memory processes that are characteristic of the Alzheimer’s disease (AD). The loss of cholinergic neurons and muscarinic receptors (MR) in the nucleus basalis of Meynert have been reported in AD. The endocannabinoid system is a neuromodulator of the BFCS, but there are controversial reports regarding the cannabinoid effects in learning and memory processes. The animal models of cholinergic impairment mimic the main histopathological and behavioral effects observed in patients. The MR antagonism, e.g. using scopolamine (SCOP), is used as a model of amnesia in rodents. The intraparenchymal administration of 192-IgG-saporin (SAP) in the nucleus basalis magnocellularis eliminates cholinergic neurons leading to learning and memory deficits. Then, the present study evaluates the modulation of spatial and working memory with the Barnes Maze following a subchronic treatment with a low dose (0.5 mg/kg) of WIN55,212-2 (WIN) in both the SCOP and SAP models of learning and memory deficit. In the SCOP model, the administration of WIN protects learning and memory impairment during the probe trial, recorded as the time spent in the target quadrant (WIN + SCOP: 78 ± 13 sec vs VEH + SCOP: 45 ± 3 sec; p < 0.001). A similar effect of the treatment was observed in the SAP model (SAP: 50 ± 3 sec vs SAP + WIN: 82 ± 7 sec; p < 0.001). This effect was specifically mediated by CB1 receptors, since it was blocked by the co-administration of the specific CB1 antagonist, SR141716A (0.5 mg/kg) (SAP: 49 ± 3 sec vs SAP + WIN + SR: 48 ± 5 sec). However, higher doses of WIN (3 mg/kg) induced negative effects in learning and memory in control (C) rats, but positive and comparable to the lower dose in the SAP model (C: 89 ± 3 sec, C + WIN-3 mg/kg: 48 ± 3 sec; SAP: 49 ± 3; SAP + WIN-3 mg/kg: 80 ± 12 sec; p < 0.001). The CB1 receptor activation by low doses of the cannabinoid agonist WIN are able to block the amnesic effects induced by SCOP and also the learning and memory impairment produced by the BFCS pathway degeneration. CB1 agonists could contribute to improve the clinical symptoms of AD. International application patent PCT/EP2018/054525.
Related Products: 192-IgG-SAP (Cat. #IT-01)