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Cholinergic Receptors: Nicotinic01:15

Cholinergic Receptors: Nicotinic

6.8K
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...
6.8K
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants

2.3K

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...
2.3K
Cholinergic Receptors: Muscarinic01:25

Cholinergic Receptors: Muscarinic

6.3K
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+....
6.3K
Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:22

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

2.6K
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...
2.6K
Direct-Acting Cholinergic Agonists: Pharmacological Actions00:59

Direct-Acting Cholinergic Agonists: Pharmacological Actions

2.6K
Direct-acting cholinergic agonists exert their pharmacological actions by mimicking the effects of acetylcholine on postsynaptic muscarinic receptors to generate parasympathetic responses. These agents elicit a range of physiological responses, including cardiovascular effects. For example, activation of muscarinic receptors induces bradycardia, decreased cardiac output, reduced peripheral resistance, and consequent hypotension. In the eye, stimulation of M3 receptors leads to smooth muscle...
2.6K
Parasympathetic Signaling01:30

Parasympathetic Signaling

4.3K
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...
4.3K

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Related Experiment Video

Updated: Apr 17, 2026

The 5-Choice Serial Reaction Time Task: A Task of Attention and Impulse Control for Rodents
09:43

The 5-Choice Serial Reaction Time Task: A Task of Attention and Impulse Control for Rodents

Published on: August 10, 2014

47.3K

Nicotinic receptors and attention.

Britta Hahn1

  • 1Maryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore, MD, USA, bhahn@mprc.umaryland.edu.

Current Topics in Behavioral Neurosciences
|February 7, 2015
PubMed
Summary

Nicotinic acetylcholine receptor (nAChR) agonists enhance attention, offering therapeutic potential for cognitive disorders. Research identifies noradrenaline and glutamate as key mediators, guiding the development of selective nAChR drugs.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cognitive Science

Background:

  • Nicotinic acetylcholine receptor (nAChR) agonists show promise for treating cognitive deficits in conditions like Alzheimer's disease and schizophrenia.
  • Nicotine, a nonselective nAChR agonist, enhances attention in humans and animals, suggesting broader therapeutic applications beyond smoking cessation.

Purpose of the Study:

  • To elucidate the neuronal mechanisms underlying the attention-enhancing effects of nAChR agonists.
  • To identify specific nAChR subtypes and secondary neurotransmitter systems critical for attention.
  • To guide the development of selective nAChR-targeting compounds with improved therapeutic profiles and minimized side effects.

Main Methods:

  • Review of preclinical and human studies investigating nAChR agonist effects on attention.

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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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Last Updated: Apr 17, 2026

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The 5-Choice Serial Reaction Time Task: A Task of Attention and Impulse Control for Rodents

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Touchscreen Sustained Attention Task SAT for Rats
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Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine
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  • Analysis of neurotransmitter systems (noradrenaline, glutamate, dopamine) involved in mediating nicotine's pro-attentional effects.
  • Examination of neuroimaging data to understand how nAChR agonists modulate brain activity during attention tasks.
  • Main Results:

    • Noradrenaline and glutamate release, but not dopamine, are critical mediators of nicotine's attention-enhancing effects.
    • nAChR agonists modulate diverse brain systems, impacting activation and deactivation patterns during attention tasks.
    • Distinct central mechanisms likely underlie the effects of nAChR agonists on different attentional functions.

    Conclusions:

    • Selective nAChR agonists targeting specific subtypes could offer therapeutic benefits for cognitive impairments.
    • Understanding the interaction between nAChRs and secondary neurotransmitter systems is crucial for developing effective treatments.
    • Future drug development should focus on achieving precise modulation of specific nAChR subtypes to optimize attentional function.