ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
TrkA gene ablation in basal forebrain results in dysfunction of the cholinergic circuitry.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 98 citations in OpenAlex.
- Multimodal beneficial effects of BNN27, a nerve growth factor synthetic mimetic, in the 5xFAD mouse model of Alzheimer's disease.Molecular psychiatry · 2025Article
- Projections from ventral hippocampus to nucleus accumbens' cholinergic neurons are altered in depression.The Journal of general physiology · 2025Article
- Utility of a commercial antibody against NTRK1 for western blotting and potential application to immunohistochemistry in adult mouse brain.Scientific reports · 2025Article
- The state of the art in secondary pharmacology and its impact on the safety of new medicines.Nature reviews. Drug discovery · 2024Review
- Basal forebrain cholinergic signalling: development, connectivity and roles in cognition.Nature reviews. Neuroscience · 2023Review
- Enhanced TrkA signaling impairs basal forebrain-dependent behavior.Frontiers in molecular neuroscience · 2023Article
- A functional circuit formed by the autonomic nerves and myofibroblasts controls mammalian alveolar formation for gas exchange.Developmental cell · 2022Article
- Single cell enhancer activity distinguishes GABAergic and cholinergic lineages in embryonic mouse basal ganglia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- TrkA-cholinergic signaling modulates fear encoding and extinction learning in PTSD-like behavior.Translational psychiatry · 2022Article
- Retrograde Axonal Transport of Neurotrophins in Basal Forebrain Cholinergic Neurons.Methods in molecular biology (Clifton, N.J.) · 2022Article
- A Deficiency of the Psychiatric Risk Gene DLG2/PSD-93 Causes Excitatory Synaptic Deficits in the Dorsolateral Striatum.Frontiers in molecular neuroscience · 2022Article
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- Fatty acid mobilization from adipose tissue is mediated by CD36 posttranslational modifications and intracellular trafficking.JCI insight · 2021Article
- Role of EphA4 in Mediating Motor Neuron Death in MND.International journal of molecular sciences · 2021Review
- Co-treatment of vitamin D supplementation with enriched environment improves synaptic plasticity and spatial learning and memory in aged rats.Psychopharmacology · 2021Article
- Neurotrophin signalling in amygdala-dependent cued fear learning.Cell and tissue research · 2020Review
- Decreased number of striatal cholinergic interneurons and motor deficits in dopamine receptor 2-expressing-cell-specific Dyt1 conditional knockout mice.Neurobiology of disease · 2020Article
- Diterpene Ginkgolides Exert an Antidepressant Effect Through the NT3-TrkA and Ras-MAPK Pathways.Drug design, development and therapy · 2020Article
- The NGFThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Reduced Cholinergic Activity in the Hippocampus of Hippocampal Cholinergic Neurostimulating Peptide Precursor Protein Knockout Mice.International journal of molecular sciences · 2019Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Dysfunction of basal forebrain cholinergic neurons (BFCNs) is an early pathological hallmark of Alzheimer's disease (AD). Numerous studies have indicated that nerve growth factor (NGF) supports survival and phenotypic differentiation of BFCNs. Consistent with a potential link to AD pathogenesis, TrkA, a NGF receptor, is expressed in cholinergic forebrain neuronal populations including those in BF and striatum, and is markedly reduced in individuals with mild cognitive impairment (MCI) without dementia and early-stage AD. To investigate the role of TrkA in the development, connectivity, and function of the BF cholinergic system and its contribution to AD pathology, we have generated a forebrain-specific conditional TrkA knock-out mouse line. Our findings show a key role for TrkA signaling in establishing the BF cholinergic circuitry through the ERK pathway, and demonstrate that the normal developmental increase of choline acetyltransferase expression becomes critically dependent on TrkA signaling before neuronal connections are established. Moreover, the anatomical and physiological deficits caused by lack of TrkA signaling in BFCNs have selective impact on cognitive activity. These data demonstrate that TrkA loss results in cholinergic BF dysfunction and cognitive decline that is reminiscent of MCI and early AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.