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Related Concept Videos

Cholinergic Receptors: Nicotinic01:15

Cholinergic Receptors: Nicotinic

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...
Cholinergic Neurons: Neurotransmission01:23

Cholinergic Neurons: Neurotransmission

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...
Cholinergic Receptors: Muscarinic01:25

Cholinergic Receptors: Muscarinic

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+. Activation...
Chemical Synapses01:26

Chemical Synapses

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...
Chemical Synapses01:26

Chemical Synapses

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...
Parasympathetic Signaling01:30

Parasympathetic Signaling

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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Localization of Plasma Membrane and Intracellular Neuronal Nicotinic Acetylcholine Receptors Using Quantitative Imaging in Mammalian Cells
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Inflammatory cytokines decrease the expression of nicotinic acetylcholine receptor during the cell maturation.

Yukiko Kondo1, Eiichi Tachikawa, Shinpei Ohtake

  • 1Department of Pharmacology, Iwate Medical School, Bldg 3-4, 19-1 Uchimaru, Morioka, Iwate, 020-8505, Japan.

Molecular and Cellular Biochemistry
|July 24, 2009
PubMed
Summary

The nervous system regulates inflammation. This study found lipopolysaccharide (LPS) reduced nicotinic receptors on antigen-presenting cells (APCs), while nicotine did not affect this reduction or cytokine release.

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Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • The nervous system, particularly the parasympathetic nervous system, modulates systemic inflammatory responses.
  • The alpha 7 subunit of the nicotinic acetylcholine receptor is implicated in cholinergic inhibition of cytokine synthesis in macrophages.
  • Antigen-presenting cells (APCs) are crucial for initiating T cell responses and maintaining immunity.

Purpose of the Study:

  • To investigate the expression of nicotinic receptors on a p53-deficient APC cell line (JawsII).
  • To determine the effect of lipopolysaccharide (LPS) and tumor necrosis factor alpha (TNF-alpha) on nicotinic receptor expression and APC function.
  • To assess the impact of nicotine stimulation on cytokine release in APCs.

Main Methods:

  • Utilized a p53-deficient mouse bone marrow-derived APC cell line (JawsII).
  • Stimulated JawsII cells with lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF-alpha), and nicotine.
  • Measured CD80 and CD86 expression, surface nicotinic receptor levels, and cytokine secretion (IL-1a, IL-1b, IL-6, TNF-alpha).

Main Results:

  • LPS and TNF-alpha stimulation increased CD80 and CD86 expression on JawsII cells.
  • These inflammatory stimuli also led to a decrease in surface nicotinic receptor expression.
  • Nicotine stimulation alone did not alter CD80/CD86 expression or receptor levels.
  • LPS stimulation augmented the secretion of IL-1a, IL-1b, IL-6, and TNF-alpha.
  • Nicotinic stimulation did not prevent the LPS-induced decrease in alpha 7 nicotinic acetylcholine receptor expression.

Conclusions:

  • LPS stimulation diminishes alpha 7 nicotinic acetylcholine receptor expression on JawsII cells.
  • Nicotine stimulation does not counteract the effect of LPS on receptor expression or cytokine release.
  • These findings suggest a complex interplay between inflammatory signals and cholinergic pathways in APCs.