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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...
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...
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.
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Drugs Affecting GI Tract Motility: Dopamine Receptor Antagonists01:28

Drugs Affecting GI Tract Motility: Dopamine Receptor Antagonists

Prokinetic agents are specialized medications that stimulate gastrointestinal (GI) motility, promoting food movement through the GI tract. Dopamine, an inhibitory neurotransmitter, plays a significant role in this process, reducing GI motility and indirectly controlling the speed of digestion. Dopamine receptor antagonists, such as metoclopramide and domperidone, offer a unique advantage as prokinetic agents. By blocking the dopamine receptors, these drugs increase GI motility, improving food...
Indirect-Acting Cholinergic Agonists: Pharmacological Actions01:30

Indirect-Acting Cholinergic Agonists: Pharmacological Actions

Indirect-acting cholinergic agonists, also known as anticholinesterases, exert their pharmacological effects by enhancing cholinergic transmission in various body parts, including the neuromuscular junction, autonomic cholinergic synapses, and the brain.
At the neuromuscular junction, these agents work by inhibiting the breakdown of acetylcholine, allowing it to remain bound to the receptor and bind to nearby receptors. This process leads to repetitive firing of the endplate, causing muscle...
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 27, 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

Nicotinic cholinergic mechanisms causing elevated dopamine release and abnormal locomotor behavior.

B N Cohen1, E D W Mackey, S R Grady

  • 1Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.

Neuroscience
|November 15, 2011
PubMed
Summary

Altered alpha6 nicotinic acetylcholine receptors (nAChRs) in dopamine neurons significantly impact motor activity and dopamine release. Hypersensitive alpha6 nAChRs can cause hyperactivity, demonstrating cholinergic system control over dopamine transmission.

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Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area
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Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area

Published on: August 10, 2012

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Last Updated: May 27, 2026

Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices
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Published on: October 29, 2012

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease
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Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area
09:54

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area

Published on: August 10, 2012

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Molecular Biology

Background:

  • Dopamine (DA) neurons in the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) regulate DA release in key brain regions.
  • Cholinergic transmission, particularly via nicotinic acetylcholine receptors (nAChRs), plays a critical role in modulating DA neuron activity and DA release.

Purpose of the Study:

  • To investigate the specific role of alpha6* nAChRs in dopamine transmission.
  • To examine the behavioral and neurochemical consequences of varying levels of hypersensitive alpha6 nAChRs.

Main Methods:

  • Utilized mouse models with different copy numbers of a mutant, hypersensitive (L9'S) alpha6 nAChR subunit.
  • Assessed locomotor activity (home-cage, novelty-induced, wheel running) and nicotine-stimulated DA release from striatal synaptosomes.

Main Results:

  • Mice with high copy numbers of hypersensitive alpha6 L9'S subunits exhibited spontaneous hyperactivity and enhanced nicotine-stimulated locomotor activity.
  • High-copy alpha6 L9'S mice showed blunted wheel running, attributed to reduced running time and velocity.
  • ACh and nicotine-stimulated DA release correlated with observed behavioral changes, suggesting augmented DA release mediates altered behaviors.

Conclusions:

  • The nicotinic cholinergic system precisely controls dopamine transmission.
  • Enhanced DA release, mediated by hypersensitive alpha6* nAChRs, is linked to significant alterations in motor behavior.