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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...
Drug Dependence01:17

Drug Dependence

Medications are typically administered to achieve therapeutic effects. Some drugs can modify an individual's mood and perception, frequently resulting in various enjoyable experiences. However, this can result in drug dependency, a condition marked by continuous drug use despite potential negative consequences. Drug dependency primarily falls into two categories: psychological and physical dependence. Psychological dependence occurs when the pleasurable feelings induced by the drug...
CNS Stimulants: Cocaine, Amphetamines and Cannabinoids01:24

CNS Stimulants: Cocaine, Amphetamines and Cannabinoids

CNS stimulants, such as cocaine, amphetamines, and cannabinoids, have varying structures and mechanisms of action that lead to different therapeutic effects and side effects. Cocaine, with its molecular formula C17H21NO4, is a tropane alkaloid and a tertiary amino compound. It has two chemical forms: the hydrochloride salt and the "freebase." The former is in powder form, while the latter involves removing the hydrochloride salt to create a form that can be smoked. Cocaine exerts its effects by...
Drug Abuse and Addiction: Pharmacological Phenomena01:15

Drug Abuse and Addiction: Pharmacological Phenomena

Drug dependence, abuse, and addiction are complex phenomena that can precipitate various abnormal states. Physical dependence refers to a state of pharmacological adaptation to a drug. This adaptation often results in tolerance—a reduced response to the drug after repeated administrations. When the drug use is abruptly stopped, withdrawal symptoms occur due to the body's need to readjust from the pharmacologically induced imbalance. However, tolerance and withdrawal symptoms do not necessarily...
Opioid Receptors: Overview01:22

Opioid Receptors: Overview

Opioid receptors, including the mu (μ, MOR), delta (δ, DOR), and kappa (κ, KOR) types, belong to the rhodopsin family of G protein-coupled receptors. These receptors are located throughout the central and peripheral nervous systems and in non-neuronal tissues such as macrophages and astrocytes. Opioid receptor ligands can be categorized into agonists or antagonists. Highly selective agonists include [d-Ala2, MePhe4, Gly(ol)5]-enkephalin or DAMGO for MOR, [D-Pen2, D-Pen5]-enkephalin or DPDPE for...

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Related Experiment Video

Updated: May 23, 2026

Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons
12:19

Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons

Published on: June 24, 2015

Nicotine-induced changes of brain β-endorphin.

K P Gudehithlu1, A-M Duchemin, G A Tejwani

  • 1Department of Pharmacology, College of Medicine, The Ohio State University, Columbus, OH 43210, USA. neff.6@osu.edu

Neuropeptides
|April 10, 2012
PubMed
Summary

Nicotine impacts brain beta-endorphin levels, affecting mood and reward. This study shows nicotine alters beta-endorphin synthesis and release in key brain areas, potentially contributing to addiction.

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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

Related Experiment Videos

Last Updated: May 23, 2026

Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons
12:19

Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons

Published on: June 24, 2015

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

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Endogenous opioid peptides and their receptors are crucial for nicotine's psychoactive effects.
  • Behavioral studies suggest beta-endorphin influences nicotine's rewarding and emotional impacts.
  • The precise effect of nicotine on brain endorphinergic neuron function remains incompletely understood.

Purpose of the Study:

  • To investigate the impact of acute and chronic nicotine administration on brain beta-endorphin and its precursor, proopiomelanocortin (POMC).
  • To explore the role of specific neurochemical pathways, including dopaminergic systems, in mediating nicotine's effects on beta-endorphin.

Main Methods:

  • Administration of free base nicotine (acute and chronic 14-day regimens) to subjects.
  • Measurement of beta-endorphin content and POMC mRNA levels in various brain regions (hypothalamus, striatum, hippocampus, prefrontal cortex).
  • Assessment of the involvement of nicotinic and dopaminergic receptors using antagonists like mecamylamine and haloperidol.

Main Results:

  • Both acute and chronic nicotine treatments reduced beta-endorphin levels in the hypothalamus, striatum, and hippocampus.
  • Nicotine's acute effect on beta-endorphin was counteracted by mecamylamine and haloperidol, indicating involvement of nicotinic and dopamine D2-like receptors.
  • Chronic nicotine moderately decreased POMC mRNA in the hypothalamus and prefrontal cortex, while acute nicotine had no significant effect.
  • Pituitary and plasma beta-endorphin levels remained unaffected by nicotine treatments.

Conclusions:

  • Nicotine alters the synthesis and release of beta-endorphin within the limbic brain system in vivo.
  • These alterations in endorphinergic function may underlie the behavioral effects of nicotine.
  • Modulated endorphinergic activity could play a significant role in the development of nicotine addiction.