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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: 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...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...

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Related Experiment Video

Updated: May 9, 2026

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

Striatal dopamine transmission is reduced after chronic nicotine with a decrease in α6-nicotinic receptor control in

Richard Exley1, Michael A Clements2, Henrike Hartung3

  • 1Department of Physiology Anatomy and Genetics, University of Oxford, Sherrington Building, Oxford OX1 3PT, UK. richard.exley@dpag.ox.ac.uk

The European Journal of Neuroscience
|July 12, 2013
PubMed
Summary

Chronic nicotine exposure alters dopamine release in the brain. Nicotine addiction may stem from changes in how specific nicotinic acetylcholine receptors (nAChRs) control dopamine release, particularly in the nucleus accumbens.

Keywords:
addictionmouserewardvoltammetryα-conotoxin-MII

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

Published on: February 10, 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: May 9, 2026

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

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

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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 regulates striatal dopamine (DA) neurotransmission through presynaptic nicotinic acetylcholine receptors (nAChRs).
  • Smokers exhibit upregulated striatal nAChR density, with potential differential effects on α6- or α4-containing nAChRs.
  • Understanding these changes is crucial for addressing nicotine addiction.

Purpose of the Study:

  • To investigate how chronic nicotine exposure modifies striatal DA transmission.
  • To determine if acute nicotine's effects on DA release probability persist after chronic exposure.
  • To compare the regulation of DA release by α6-subunit-containing (α6*) versus non-α6* nAChRs in the nucleus accumbens (NAc) and caudate-putamen (CPu).

Main Methods:

  • Electrically evoked DA release was measured in striatal slices from mice.
  • Mice were exposed to nicotine (200 μg/mL in drinking water) or a control solution for 4-8 weeks.
  • Carbon-fiber microelectrodes were used to detect DA release.

Main Results:

  • Chronic nicotine exposure subtly reduced striatal DA release evoked by single pulses.
  • In the NAc, chronic nicotine enhanced the range of DA release across different frequencies.
  • In the NAc, there was a downregulation of α6α4β2β3 nAChR dominance and an emergence of non-α6* nAChR function; no such change was observed in the CPu.

Conclusions:

  • Chronic nicotine subtly modifies DA transmission regulation.
  • In the NAc, this modification involves the downregulation of α6α4β2β3 nAChR function.
  • This imbalance in α6:non-α6 nAChR function may contribute to DA dysregulation in nicotine addiction.