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The effect of nerve growth factor on supporting spatial memory depends upon hippocampal cholinergic innervation
Eu WZ, Chen YJ, Chen WT, Wu KY, Tsai CY, Cheng SJ, Carter RN, Huang GJ (2021) The effect of nerve growth factor on supporting spatial memory depends upon hippocampal cholinergic innervation. Transl Psychiatry 11(1):162. doi: 10.1038/s41398-021-01280-3
Objective: To determine whether the supportive effect of NGF on learning and memory is specifically dependent upon intact hippocampal cholinergic innervation.
Summary: The results demonstrate that the hippocampal cholinergic system is required for maintaining spatial memory function, without having an impact on anxiety.
Usage: Twelve-week-old male C57BL/6Narl mice were used for hippocampal cholinergic denervation. Mice received bilateral injections into the hippocampus; 0.2 μg of mu p75-SAP was administered per site.
Related Products: mu p75-SAP (Cat. #IT-16)
Minocycline in neurodegenerative and psychiatric diseases: An update.
Romero-Miguel D, Lamanna-Rama N, Casquero-Veiga M, Gómez-Rangel V, Desco M, Soto-Montenegro ML (2021) Minocycline in neurodegenerative and psychiatric diseases: An update. Eur J Neurol 28(3):1056-1081. doi: 10.1111/ene.14642
Summary: Review includes the mouse animal model of neurodegenerative disease using mu p75-SAP. Biological Effects: Attenuation of cholinergic neurons loss, glial activation and transcription of pro-inflammatory mediators.
Usage: 45 mg/Kg, i.p.
Related Products: mu p75-SAP (Cat. #IT-16)
Cholinergic signalling in the forebrain controls microglial phenotype and responses to systemic inflammation
Nazmi A, Griffin EW, Field RH, Doyle S, Hennessy E, O’Donnell M, Rehill A, McCarthy A, Healy D, Doran MM, Lowry JP, Cunningham C (2021) Cholinergic signalling in the forebrain controls microglial phenotype and responses to systemic inflammation. bioRxiv 2021.01.18.427123. doi: 10.1101/2021.01.18.427123
Related Products: mu p75-SAP (Cat. #IT-16)
Loss of cholinergic innervation differentially affects eNOS-mediated blood flow, drainage of Aβ and cerebral amyloid angiopathy in the cortex and hippocampus of adult mice
Nizari S, Wells JA, Carare RO, Romero IA, Hawkes CA (2021) Loss of cholinergic innervation differentially affects eNOS-mediated blood flow, drainage of Aβ and cerebral amyloid angiopathy in the cortex and hippocampus of adult mice. Acta Neuropathol Commun 9(1):12. doi: 10.1186/s40478-020-01108-z
Summary: In this report, icv administration of mu p75-SAP resulted in significant death of cholinergic neurons and fibres in the medial septum, cortex and hippocampus of C57BL/6 mice. This study supports the importance of the interrelationship between cholinergic innervation and vascular function in the etiology and/or progression of cerebral amyloid angiopathy (CAA) and suggests that combined endothelial nitric oxide synthase (eNOS)/cholinergic therapies may improve the efficiency of Aβ removal from the brain and reduce its deposition as CAA.
Usage: mu p75-SAP (0.596 μg/μl) was injected into the left and right lateral ventricles.
Related Products: mu p75-SAP (Cat. #IT-16)
Identification of multiple targets in the fight against Alzheimer’s disease
Giannoni P, Fossati S, Claeysen S, Marcello E, eds (2020) Identification of multiple targets in the fight against Alzheimer’s disease. Front Aging Neurosci 12:169. doi: 10.3389/fnagi.2020.00169
Summary: A collection of 20 articles that depict a broad representation of the most impactful advances in Alzheimer’s disease (AD) comprehension and therapeutic openings.
Related Products: 192-IgG-SAP (Cat. #IT-01), mu p75-SAP (Cat. #IT-16)
In vivo monitoring of cholinergic neurotransmission with a microelectrochemical choline biosensor
Cunningham C, Lowry JP (2019) In vivo monitoring of cholinergic neurotransmission with a microelectrochemical choline biosensor. Neuroscience 2019 Abstracts 614.03. Society for Neuroscience, Chicago, IL.
Summary: Acetylcholine acts as a key neuromodulator within the central nervous system, capable of altering neuronal excitability and coordinating neuronal firing patterns. Conversely, cholinergic neurotransmission plays a crucial role in a variety of cognitive functions, including the encoding of new memories. Cholinergic neuronal loss, and the resulting drop in cholinergic neurotransmission (collectively referred to as hypocholinergia), is closely associated with cognitive dysfunction in a number of chronic neurodegenerative disorders including Alzheimer’s disease. However, conventional analytical techniques for monitoring in vivo cholinergic neurotransmission lack the spatiotemporal resolution required to accurately detect endogenous cholinergic dynamics. Here we validate in mice a Pt-based electrochemical biosensor for selective monitoring of choline, a verified marker of cholinergic transmission. Enzymatic choline biosensors (modified with choline oxidase) were sterotaxically implanted in the medial prefrontal cortex (mPFC) and contralateral dorsal hippocampus (dHPC) of female C57Bl6J mice. Real-time choline current recordings over a period of several days revealed circadian fluctuations in both regions, with extracellular choline levels highest during light phases. Administration of pharmacological compounds known to induce central acetylcholine release, scopolamine (1mg/kg) and amphetamine (4mg/kg), evoked a robust increase in choline current. In contrast, peripheral injection of the reversible acetylcholinesterase inhibitor, donepezil (3mg/kg), produced a marked decrease in recorded choline current. The induction of systemic infammation with bacterial lipopolysaccharide (LPS; 500µg/kg) produced characteristic ‘sickness behaviour’ in mice and evoked a tonic rise in central choline levels in both the mPFC and dHPC. Furthermore, the induction of hypocholinergia in selected mice was preformed via intracerebroventricular injections of murine-p75-saporin immunotoxin (1.2µg). Evoked cholinergic neurotransmission was dramatically attenuated in lesioned (hypocholinergic) mice. Collectively, the data suggests that microelectrochemical choline biosensors may serve as a powerful tool for monitoring cholinergic neurotransmission across a number of behavioural and disease states.
Related Products: mu p75-SAP (Cat. #IT-16)
Role of nociceptive afferent input on forelimb reaching and grasping behaviors in the spinal cord injured rat
Walker JR, Ong A, Detloff MR (2019) Role of nociceptive afferent input on forelimb reaching and grasping behaviors in the spinal cord injured rat. Neuroscience 2019 Abstracts 572.09. Society for Neuroscience, Chicago, IL.
Summary: Individuals with spinal cord injury (SCI) suffer a loss of motor and sensory function. The current standard of care to recover fine motor control is rehabilitation focused on a combination of range of motion, aerobic, and strength training (ST). However, limited research has been conducted to determine the role of nociceptive afferent inputs from muscle on spinal plasticity and/or recovery of function. Using a rodent model of SCI strength training rehabilitation, we determined that motor training not only improves forelimb strength and fine motor function but also can modulate the development of neuropathic pain, suggesting that improvements in reaching and grasping may be due, in part, to plasticity of nociceptive afferents. To further explore this, Sprague-Dawley rats received injections of rIB4-conjugated saporin, mu p75-conjugated saporin or unconjugated (vehicle) into the cervical dorsal root ganglia unilaterally to eliminate non-peptidergic and peptidergic nociceptors. There is an uninjured cohort and a group with unilateral C5 SCI. Von Frey and Hargreaves’ tests were performed at baseline and several time points post-injection to assess the effcacy of the nociceptive elimination. Several measures of forelimb strength were recorded over time including the isometric pull task, a single pellet retrieval task and the Montoya staircase test. To confirm the depletion of peptidergic and non-peptidergic nociceptors following saporin injection and/or SCI, cervical DRGs and spinal cords were stained with antibodies against CGRP and isolectin-B4. An understanding of the role of nociceptors in spinal plasticity and functional motor and sensory recovery of SCI patients will guide future research and refine rehabilitation strategies to further improve their quality of life.
Related Products: IB4-SAP (Cat. #IT-10), mu p75-SAP (Cat. #IT-16)
3D reconstruction of the neurovascular unit reveals differential loss of cholinergic innervation in the cortex and hippocampus of the adult mouse brain.
Nizari S, Carare RO, Romero IA, Hawkes CA (2019) 3D reconstruction of the neurovascular unit reveals differential loss of cholinergic innervation in the cortex and hippocampus of the adult mouse brain. Front Aging Neurosci 11:172. doi: 10.3389/fnagi.2019.00172
Objective: To further characterize the effect of the loss of cholinergic innervation on the NVU (neurovascular unit) in Alzheimer’s Disease.
Summary: Significantly less ChAT staining was detected in the medial septum of saporin-treated mice at 45 days post-surgery. This was accompanied by a significant decrease in cholinergic nerve fiber density in the hippocampus and the cortex. As expected, p75 NTR-negative neurons in the striatum were not affected by mu p75-SAP treatment.
Usage: In this study, the mu-p75-SAP was used to induce death of basal forebrain cholinergic neurons and their fiber projections. mu p75-SAP 0.5 µL (0.596 µg/µL) or 0.9% saline (n = 19) was injected into each ventricle.
Related Products: mu p75-SAP (Cat. #IT-16)
Central cholinergic neuronal degeneration promotes the development of postoperative cognitive dysfunction.
Xu H, Chen L, Zhang X, Jiang X, Tian W, Yu W, Wang X, Tian J, Su D (2019) Central cholinergic neuronal degeneration promotes the development of postoperative cognitive dysfunction. Lab Invest 99(7):1078-1088. doi: 10.1038/s41374-018-0174-9
Usage: 1 microliter of mu-p75-SAP at a concentration of 0.8 μg/μl was injected into the lateral ventricles.
Related Products: mu p75-SAP (Cat. #IT-16)
Removal of p75 neurotrophin receptor expression from cholinergic basal forebrain neurons reduces amyloid-β plaque deposition and cognitive impairment in aged APP/PS1 mice.
Qian L, Milne MR, Shepheard S, Rogers ML, Medeiros R, Coulson EJ (2019) Removal of p75 neurotrophin receptor expression from cholinergic basal forebrain neurons reduces amyloid-β plaque deposition and cognitive impairment in aged APP/PS1 mice. Mol Neurobiol 56(7):4639-4652. doi: 10.1007/s12035-018-1404-2
Objective: To investigate the contribution of CBF neuronal p75NTR to the progression of Alzheimer’s Disease
Summary: Data indicate that a direct interaction between CBF-expressed p75NTR and Aβ does not contribute significantly to the regulation of Aβ load.
Usage: To lesion CBF neurons, a single infusion of mu p75-SAP or control Rabbit IgG-SAP (0.4 mg/ml) was stereotaxically-injected into the basal forebrain.
Related Products: mu p75-SAP (Cat. #IT-16), Rabbit IgG-SAP (Cat. #IT-35)