ArticleNeurobiology of aging2008
Regulation of the NMDA receptor-mediated synaptic response by acetylcholinesterase inhibitors and its impairment in an animal model of Alzheimer's disease.
Article in Neurobiology of aging, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- The effect of acetylcholinesterase inhibitor rivastigmine in pentylenetetrazole-induced kindling model of epilepsy in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Effects of extracts and manna ofResearch in pharmaceutical sciences · 2024Article
- Long-Term Acetylcholinesterase Depletion Alters the Levels of Key Synaptic Proteins while Maintaining Neuronal Markers in the Aging Zebrafish (Danio rerio) Brain.Gerontology · 2023Article
- Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications.Molecular psychiatry · 2022Review
- Involvement of Cholinergic, Adrenergic, and Glutamatergic Network Modulation with Cognitive Dysfunction in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Timing of repetition suppression of event-related potentials to unattended objects.The European journal of neuroscience · 2020Article
- Protrudin modulates seizure activity through GABACell death & disease · 2019Article
- Psoralidin Stimulates Expression of Immediate-Early Genes and Synapse Development in Primary Cortical Neurons.Neurochemical research · 2018Article
- Chronic nicotine differentially affects murine transcriptome profiling in isolated cortical interneurons and pyramidal neurons.BMC genomics · 2017Article
- Modulation of AMPA receptor mediated current by nicotinic acetylcholine receptor in layer I neurons of rat prefrontal cortex.Scientific reports · 2015Article
- Glutamate Receptor Modulation Is Restricted to Synaptic Microdomains.Cell reports · 2015Article
- Septo-hippocampo-septal loop and memory formation.Basic and clinical neuroscience · 2013Review
- Pharmacological effects of 3-iodothyronamine (T1AM) in mice include facilitation of memory acquisition and retention and reduction of pain threshold.British journal of pharmacology · 2013Article
- NMDA Neurotransmission Dysfunction in Behavioral and Psychological Symptoms of Alzheimer's Disease.Current neuropharmacology · 2012Article
- Aging of the NMDA receptor: from a mouse's point of view.Future neurology · 2012Article
- Restoration of synaptic plasticity and learning in young and aged NCAM-deficient mice by enhancing neurotransmission mediated by GluN2A-containing NMDA receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Selective Vulnerabilities of N-methyl-D-aspartate (NMDA) Receptors During Brain Aging.Frontiers in aging neuroscience · 2010Article
- Amyloid beta mediates memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2009Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The cholinergic system is crucial for cognitive processes and the deficient acetylcholine (ACh) function has been implicated in Alzheimer's disease (AD). Inhibitors of acetylcholinesterase (AChE), which act to enhance cholinergic function by prolonging the action of endogenously released ACh, have been used as the major therapy of AD. To understand the functional roles of cholinergic enhancement in prefrontal cortex (PFC), a key brain region for cognition, we examined the impact of AChE inhibitors in PFC neurons on synaptic responses mediated by the NMDA receptor (NMDAR), an important player in learning and memory. We found that AChE inhibitors produced a strong and persistent reduction of the amplitude of NMDA receptor-mediated excitatory postsynaptic current (NMDAR-EPSC). This effect was mainly mediated by nicotinic ACh receptors, and through a Ca(2+)-dependent mechanism. Inhibition of extracellular signal-regulated kinases (ERK) abolished the regulation of NMDAR function by AChE inhibitors, suggesting the involvement of ERK. In the transgenic mouse model of AD overexpressing mutant beta-amyloid precursor protein (APP), the effect of AChE inhibitors on NMDAR-EPSC was significantly impaired, which was associated with their diminished effect on ERK activation. Taken together, these results suggest that one of the key targets of endogenous ACh involved in cognition is the NMDAR-mediated transmission. Loss of the regulation of synaptic NMDAR responses by endogenous ACh may contribute to the cognitive deficiency in AD.
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