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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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Adrenergic Receptors: β Subtype01:26

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β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
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Heart Failure Drugs: β-Blockers01:22

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β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
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Cholinergic Receptors: Muscarinic01:25

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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. 
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G-Protein Gated Ion Channels01:21

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GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory...
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Sympathetic Signaling01:31

Sympathetic Signaling

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Sympathetic signaling, a vital part of the autonomic nervous system, plays a crucial role in mobilizing the body's resources in response to stress or emergencies. It involves the transmission of nerve impulses from sympathetic preganglionic fibers to postganglionic fibers. This results in the release of specific neurotransmitters and activation of adrenergic receptors.
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Related Experiment Video

Updated: Nov 11, 2025

Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration
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Cardiac nicotinic receptors show β-subunit-dependent compensatory changes.

Katarina Targosova1, Matej Kucera1, Zuzana Kilianova1,2

  • 1Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University in Bratislava, Bratislava, Slovakia.

American Journal of Physiology. Heart and Circulatory Physiology
|March 26, 2021
PubMed
Summary

Cardiac nicotinic receptors (NRs) show subunit plasticity. Missing β4 NR subunits increased β2 NR subunit mRNA, suggesting compensatory changes impacting heart rate and acetylcholine response.

Keywords:
cardiac cholinergic systemheart physiologynicotinic receptorreceptor plasticity

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Area of Science:

  • Cardiovascular Physiology
  • Neuropharmacology
  • Molecular Biology

Background:

  • Nicotinic receptors (NRs) are crucial for heart function.
  • A hypothesis suggests β2 and β4 NR subunits may be interchangeable in the heart.
  • Understanding NR subunit plasticity is key to cholinergic regulation of the heart.

Purpose of the Study:

  • To investigate the interchangeability of β2 and β4 NR subunits in the heart at the mRNA level.
  • To examine the physiological consequences of lacking specific β NR subunits on heart function.
  • To explore compensatory changes in cholinergic signaling pathways.

Main Methods:

  • Utilized mutant mice lacking β2 or β4 NR subunits.
  • Assessed mRNA expression of NR subunits and cholinergic molecules.
  • Performed isolated heart perfusions using the Langendorff method.
  • Stimulated hearts under basal, cholinergic, and adrenergic conditions.

Main Results:

  • Lack of β2 NR subunits decreased β4 and α3 subunit mRNA; increased M3 and decreased M4 muscarinic receptors.
  • Hearts lacking β2 NR subunits showed altered heart rate responses to cholinergic stimulation.
  • Lack of β4 NR subunits increased β2 subunit mRNA, decreased acetylcholine synthesis enzyme and M1/M4 muscarinic receptor mRNA.
  • β4 NR subunit deficiency led to increased basal heart rate and impaired acetylcholine response during adrenergic stimulation.

Conclusions:

  • Confirmed subunit-dependent compensatory changes in cardiac NRs.
  • Supported the hypothesis of β NR subunit plasticity, dependent on the specific missing subunit.
  • Demonstrated physiological consequences of NR subunit alterations on heart function.