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Related Concept Videos

Drugs Acting on Autonomic Ganglia: Stimulants01:23

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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...
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Adrenergic Neurons: Neurotransmission01:27

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Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
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Cholinergic Receptors: Nicotinic01:15

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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.
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Adrenergic Receptors: β Subtype01:26

Adrenergic Receptors: β Subtype

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β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
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Neurochemical Transmission: Sites of Drug Action01:26

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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...
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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

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Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices
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β2 nAChR Activation on VTA DA Neurons Is Sufficient for Nicotine Reinforcement in Rats.

Noah B Walker1, Yijin Yan1, Melissa A Tapia1

  • 1Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157.

Eneuro
|May 16, 2023
PubMed
Summary

Selective activation of beta2-containing nicotinic acetylcholine receptors (nAChRs) in the VTA is sufficient for nicotine reinforcement. This study shows that enhancing these receptors enables nicotine self-administration at low doses.

Keywords:
acetylcholineaddictiondopaminenicotinereinforcementtobacco

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Combined Infusion and Stimulation with Fast-Scan Cyclic Voltammetry CIS-FSCV to Assess Ventral Tegmental Area Receptor Regulation of Phasic Dopamine
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Area of Science:

  • Neuroscience
  • Pharmacology
  • Addiction Research

Background:

  • Nicotinic acetylcholine receptors (nAChRs) in the mesolimbic dopamine (DA) pathway are crucial for nicotine reinforcement.
  • The sufficiency of selective nAChR activation within this pathway for supporting nicotine reinforcement remains unclear.

Purpose of the Study:

  • To test if activating beta2-containing (β2*) nAChRs on VTA neurons is sufficient for nicotine self-administration (SA).
  • To investigate the role of VTA β2* nAChRs in supporting nicotine reinforcement behavior.

Main Methods:

  • Genetically modified Sprague Dawley rats to express hypersensitive β2 nAChR subunits (β2Leu9'Ser) in the VTA.
  • Assessed nicotine SA at various doses (1.5 and 30 μg/kg/infusion).
  • Used TH-Cre rats for cell-specific viral expression in VTA DA neurons and performed electrophysiological recordings.

Main Results:

  • Rats expressing β2Leu9'Ser acquired nicotine SA at a significantly lower dose (1.5 μg/kg/inf) than controls.
  • Nicotine SA was confirmed as reinforcing via saline substitution.
  • Selective expression in VTA DA neurons also supported SA at the low dose.
  • Electrophysiological data showed altered DA release dynamics in the NAc.

Conclusions:

  • Activation of β2* nAChRs on VTA neurons is sufficient to support nicotine reinforcement behavior.
  • This provides critical insight into the neurobiological mechanisms underlying nicotine addiction.
  • Targeting VTA β2* nAChRs may offer novel therapeutic strategies for smoking cessation.