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Related Concept Videos

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...
CNS Depressants: Alcohol and Nicotine01:27

CNS Depressants: Alcohol and Nicotine

Ethanol, a clear colorless alcohol, has been consumed by humans for millennia, but its effects on the body are far from benign. At lower doses, it induces decreased inhibitions and loquaciousness, leading to its social appeal. However, it can cause severe consequences at higher doses, such as coma and respiratory depression, due to its zero-order elimination kinetics. Chronic ethanol abuse wreaks havoc on multiple organ systems, particularly the CNS and the liver. Abrupt cessation of ethanol...
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...
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...
Drug-Receptor Interaction: Agonist01:25

Drug-Receptor Interaction: Agonist

Agonists are drugs that interact with specific receptors in the body to produce a biological response. When an agonist binds to a receptor, it activates or enhances the receptor's function, leading to physiological effects. The interaction between agonist drugs and receptors is crucial for their therapeutic action in various medical treatments.
Agonists can bind to receptors in different ways. Some agonists bind directly to the receptor's active site, mimicking the endogenous ligand's action.
Drugs Acting on Autonomic Ganglia: Blockers01:28

Drugs Acting on Autonomic Ganglia: Blockers

Ganglionic blockers inhibit autonomic activity by blocking nicotinic receptors in the autonomic ganglia, suppressing impulse transmission. These blockers lack selectivity between sympathetic and parasympathetic ganglia and are ineffective as neuromuscular junction antagonists. They can be categorized into two groups:

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Related Experiment Video

Updated: Jul 9, 2026

Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration
08:47

Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration

Published on: February 10, 2012

Metabotropic glutamate 5 receptor (mGluR5) antagonists decrease nicotine seeking, but do not affect the reinforcement

Matthew I Palmatier1, Xiu Liu, Eric C Donny

  • 1Department of Psychology, University of Pittsburgh, Pittsburgh, PA, USA. mattyp@ksu.edu

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology
|November 30, 2007
PubMed
Summary

Metabotropic glutamate 5 receptor (mGluR5) antagonists reduced nicotine intake and its reinforcement-enhancing effects. However, these antagonists did not alter 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

Published on: October 29, 2012

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

Published on: January 25, 2019

Related Experiment Videos

Last Updated: Jul 9, 2026

Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration
08:47

Spectral Confocal Imaging of Fluorescently tagged Nicotinic Receptors in Knock-in Mice with Chronic Nicotine Administration

Published on: February 10, 2012

Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices
10:04

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

Published on: October 29, 2012

Probing Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices via Laser Flash Photolysis of Photoactivatable Nicotine
10:48

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

Published on: January 25, 2019

Area of Science:

  • Neuroscience
  • Pharmacology
  • Addiction Research

Background:

  • Nicotine self-administration models often focus on primary reinforcement.
  • The reinforcement-enhancing effects of nicotine are less frequently studied in therapeutic development.
  • Metabotropic glutamate 5 receptors (mGluR5) are implicated in drug reinforcement.

Purpose of the Study:

  • To investigate the role of mGluR5 antagonists in nicotine's primary reinforcement and reinforcement-enhancing effects.
  • To determine if mGluR5 antagonism affects nicotine intake and its ability to enhance the value of other rewards.

Main Methods:

  • Rats underwent self-administration procedures with concurrent access to nicotine and a visual stimulus (VS).
  • Noncompetitive mGluR5 antagonists (MPEP and MTEP) were administered as pretreatment.
  • Nicotine intake and responding for VS were measured under different conditions.

Main Results:

  • MPEP and MTEP decreased both nicotine intake and the enhanced responding for the concurrently available VS.
  • Nicotine's reinforcement-enhancing effect was demonstrated by increased VS lever responding compared to a VS-only group.
  • Experimenter-administered nicotine infusions sustained the reinforcement-enhancing effect, which was not altered by MPEP or MTEP.

Conclusions:

  • mGluR5 receptors mediate nicotine seeking (primary reinforcement).
  • mGluR5 antagonism does not alter the reinforcement-enhancing effects of nicotine.
  • These findings contribute to understanding the neurobiological mechanisms of nicotine addiction and potential therapeutic targets.