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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...
Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:22

Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship

Cholinergic agonists or cholinomimetics mimic the action of acetylcholine to stimulate the parasympathetic nervous system. They are categorized into direct-acting and indirect-acting agents. The direct-acting cholinergic drugs induce the parasympathetic response by directly binding to the muscarinic or nicotine receptors. In comparison, the indirect-acting cholinergic drugs prevent acetylcholine hydrolysis, indirectly contributing to the extended parasympathetic response.
The direct-acting...
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...
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants


Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
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...

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Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine
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Caffeine and nicotine decrease acetylcholine receptor clustering in C2C12 myotube culture.

Kaia Kordosky-Herrera1, Wade A Grow

  • 1Department of Anatomy, Arizona College of Osteopathic Medicine, Midwestern University, 19555 N. 59th Avenue, Glendale, AZ 85308, USA.

Cell and Tissue Research
|November 13, 2008
PubMed
Summary

Caffeine and nicotine exposure significantly reduces acetylcholine receptor (AChR) clustering during skeletal muscle development. This may impair neuromuscular synapse formation in developing fetuses.

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Biology

Background:

  • Agrin signaling is crucial for acetylcholine receptor (AChR) clustering at neuromuscular junctions during development.
  • Environmental factors can influence skeletal muscle development and synapse formation.

Purpose of the Study:

  • To investigate the effects of caffeine and nicotine on AChR clustering in C2C12 myotubes.
  • To determine the impact of short-term and long-term exposure to these agents on both agrin-induced and spontaneous AChR clustering.

Main Methods:

  • Utilized C2C12 cell cultures to model skeletal muscle development.
  • Exposed cells to physiologically relevant concentrations of caffeine, nicotine, or both, for short-term (48h) and long-term (2 weeks) periods.
  • Quantified both agrin-induced and spontaneous AChR clustering frequencies.

Main Results:

  • Both short-term and long-term exposure to caffeine or nicotine significantly decreased agrin-induced AChR clustering.
  • Long-term exposure to caffeine or nicotine, but not short-term, significantly decreased spontaneous AChR clustering.
  • Combined exposure to caffeine and nicotine did not produce a greater inhibitory effect than individual exposures.

Conclusions:

  • Physiologically relevant concentrations of caffeine and nicotine impair AChR clustering during skeletal muscle development.
  • Prenatal exposure to caffeine or nicotine may lead to improper neuromuscular synapse formation.