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Related Concept Videos

Cholinergic Receptors: Nicotinic01:15

Cholinergic Receptors: Nicotinic

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Nicotinic receptors are ligand-gated ion channels that are activated by acetylcholine and nicotine. Upon activation, they cause a rapid increase in the permeability of cells to K+, Na+, and Ca2+, followed by depolarization and excitation. They are in the autonomic ganglia, skeletal neuromuscular junction, CNS, and adrenal medulla.
There are two types of nicotinic receptors: neuromuscular (NM/NM/N1) and neuronal (NN/NN/N2). The two families differ based on their location and selectivity to...
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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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Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

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Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
3.7K
Parasympathetic Signaling01:30

Parasympathetic Signaling

3.0K
Parasympathetic signaling plays a crucial role in regulating various physiological processes. It involves the release of acetylcholine (ACh) by parasympathetic neurons, which can have localized and short-lived effects. The majority of ACh released is rapidly inactivated at the synapse by the enzyme acetylcholinesterase (AChE), which hydrolyzes Ach into choline and acetate. Additionally, the tissue cholinesterase deactivates any ACh diffusing into the surrounding tissues.
The effects of...
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Cholinergic Neurons: Neurotransmission01:23

Cholinergic Neurons: Neurotransmission

5.0K
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...
5.0K
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

3.4K
Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
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Related Experiment Video

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Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue
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Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

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Nicotinic Acetylcholine Receptor-Mediated Metabotropic Signalling in Human Microglia.

Lydia J Bye1, Marnie L Maddock1, Rocio K Finol-Urdaneta1

  • 1Molecular Horizons, School of Medical, Indigenous and Health Sciences, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia.

Journal of Neurochemistry
|November 14, 2025
PubMed
Summary

This study reveals novel nicotinic acetylcholine receptor (nAChR) signaling in human microglia. Acetylcholine (ACh) activates intracellular calcium pathways, offering new targets for neuroinflammation therapies.

Keywords:
G‐proteinsacetylcholineinositol trisphosphateintracellular calcium concentrationmetabotropic signallingmicroglianeuroinflammationnicotinic acetylcholine receptorsphospholipase Csensitization

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Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine
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Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine

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Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices
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Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices

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Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine
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Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices
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Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Nicotinic acetylcholine receptors (nAChRs) are primarily known as ion channels in the nervous system.
  • Their function in non-neuronal cells like microglia remains less understood due to detection challenges.
  • Investigating nAChRs in microglia could illuminate mechanisms of cholinergic modulation in neuroinflammation.

Purpose of the Study:

  • To investigate nAChR-mediated intracellular signaling pathways in human microglia.
  • To explore how acetylcholine (ACh) influences microglial function and neuroinflammation.
  • To characterize the specific nAChR subunits and signaling cascades involved.

Main Methods:

  • Verified transcript expression of nAChR subunits (α7, α9, α10) in human C06 microglia.
  • Measured intracellular calcium ([Ca2+]i) changes in response to ACh using pharmacological inhibitors (U73122, 2-APB).
  • Assessed the role of extracellular calcium and internal calcium stores in ACh-induced responses.

Main Results:

  • Human microglia express nAChR subunits α7, α9, and α10.
  • ACh triggered intracellular calcium release via phospholipase C (PLC) and inositol 1,4,5-trisphosphate (IP3) pathways, independent of muscarinic activity.
  • Extracellular calcium is essential for replenishing internal stores, and repeated ACh exposure led to sensitization of microglial responses.

Conclusions:

  • Uncovered previously unrecognized nAChR signaling pathways in human microglia.
  • Demonstrated nAChR-mediated metabotropic signaling involving intracellular calcium mobilization.
  • Findings suggest potential therapeutic strategies targeting microglial nAChRs to suppress neuroinflammation.