ReviewFrontiers in molecular neuroscience2021
Cholinesterases in Tripartite Neuromuscular Synapse.
Review in Frontiers in molecular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Unlocking the Potential of Isatin Scaffolds in Acetylcholinesterase Inhibition.Archiv der Pharmazie · 2026Review
- TEMPOL Enhances Polyethylene Glycol Axon Fusion Following Sciatic Nerve Transection in Adult Rats.ACS chemical neuroscience · 2026Article
- The Central Cholinergic Synapse: A Primer.International journal of molecular sciences · 2025Review
- Fluorometric and Colorimetric Biosensors for the Assay of Cholinesterase Inhibitors.Sensors (Basel, Switzerland) · 2025Review
- Impairment of Skeletal Muscle Contraction by Inhibitors of GABA Transporters.International journal of molecular sciences · 2024Article
- Review
- A method to investigate muscle target-specific transcriptional signatures of single motor neurons.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Bringing synapses into focus: Recent advances in synaptic imaging and mass-spectrometry for studying synaptopathy.Frontiers in synaptic neuroscience · 2023Review
- The role of butyrylcholinesterase in the regulation of cognitive dysfunction in minimal hepatic encephalopathy: A potential blood marker of disease evolution.Frontiers in neurology · 2022Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuromuscular junction (NMJ) is a tripartite synapse in which not only presynaptic and post-synaptic cells participate in synaptic transmission, but also terminal Schwann cells (TSC). Acetylcholine (ACh) is the neurotransmitter that mediates the signal between the motor neuron and the muscle but also between the motor neuron and TSC. ACh action is terminated by acetylcholinesterase (AChE), anchored by collagen Q (ColQ) in the basal lamina of NMJs. AChE is also anchored by a proline-rich membrane anchor (PRiMA) to the surface of the nerve terminal. Butyrylcholinesterase (BChE), a second cholinesterase, is abundant on TSC and anchored by PRiMA to its plasma membrane. Genetic studies in mice have revealed different regulations of synaptic transmission that depend on ACh spillover. One of the strongest is a depression of ACh release that depends on the activation of α7 nicotinic acetylcholine receptors (nAChR). Partial AChE deficiency has been described in many pathologies or during treatment with cholinesterase inhibitors. In addition to changing the activation of muscle nAChR, AChE deficiency results in an ACh spillover that changes TSC signaling. In this mini-review, we will first briefly outline the organization of the NMJ. This will be followed by a look at the role of TSC in synaptic transmission. Finally, we will review the pathological conditions where there is evidence of decreased AChE activity.
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