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Cholinergic Receptors: Muscarinic01:25

Cholinergic Receptors: Muscarinic

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The pharmacological actions of acetylcholine are elicited via its binding to two families of cholinergic receptors or cholinoceptors, namely, muscarinic and nicotinic receptors. Muscarinic receptors are G protein-coupled receptors and have five subtypes, M1–M5. All mAChR subtypes are activated by acetylcholine and blocked by the antagonist, atropine. 
The subtypes M1, M3, and M5 couple with the Gq subunit and activate the phospholipase C (PLC) activity, mobilizing intracellular Ca2+....
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Chemical Synapses01:26

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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
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Cholinergic Neurons: Neurotransmission01:23

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Cholinergic neurotransmission involves the synthesis and the release of acetylcholine (ACh) in order to transmit nerve impulses across the synapse. The process begins with the synthesis of acetyl CoA, a precursor for ACh, from ATP, acetate, and coenzyme A in the mitochondria. Choline, another vital precursor, is transported inside the neuron through choline transporters, including high-affinity choline transporter CHT1, low-affinity choline transporter CTL1, and lower-affinity choline...
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Myasthenia Gravis: Overview and Treatment01:20

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Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
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Mitogens and the Cell Cycle02:38

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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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Updated: Jul 10, 2025

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

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Acetylcholine, Another Factor in Breast Cancer.

Juan P Muñoz1, Gloria M Calaf2

  • 1Laboratorio de Bioquímica, Departamento de Química, Facultad de Ciencias, Universidad de Tarapacá, Arica 1000007, Chile.

Biology
|November 24, 2023
PubMed
Summary

Acetylcholine (ACh) promotes breast cancer cell proliferation and estrogen receptor alpha (ERα) activity. This neurotransmitter may play a role in cancer progression through a ligand-independent mechanism.

Keywords:
acetylcholinebreast cancerestrogen receptor alphaestrogensmuscarinic receptor

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Area of Science:

  • Neuroscience
  • Oncology
  • Molecular Biology

Background:

  • Acetylcholine (ACh) is a neurotransmitter with a controversial role in cancer progression.
  • Previous studies linked organophosphorus pesticides to increased ACh levels and mammary tumors.
  • ACh exposure induced estrogen receptor alpha (ERα) overexpression in breast cancer cells.

Purpose of the Study:

  • To investigate the hypothesis that ACh alters ERα activity via a ligand-independent mechanism.
  • To elucidate the signaling pathways and cellular effects of ACh in breast cancer.

Main Methods:

  • Exposure of breast cancer cell lines to physiological concentrations of ACh.
  • Analysis of calcium release, MAPK/ERK and PI3K/Akt pathway activation.
  • Assessment of phosphorylated ERα (p-ERα) nuclear translocation.
  • Evaluation of estrogen-responsive gene expression and cell viability.
  • Investigation of epithelial-mesenchymal transition (EMT) marker expression.

Main Results:

  • ACh triggered Ca+2 release and activated MAPK/ERK and PI3K/Akt pathways.
  • ACh induced p-ERα and its nuclear recruitment, but not estrogen-responsive gene overexpression.
  • ACh enhanced breast cancer cell viability in an ERα-dependent manner.
  • ACh promoted the overexpression of certain EMT markers.

Conclusions:

  • ACh promotes breast cancer cell proliferation and ERα activity, potentially through a ligand-independent pathway.
  • ACh's role in ERα activation differs from 17ß-estradiol.
  • ACh may contribute to breast cancer progression by influencing ERα activity and EMT.