Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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 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:
Adrenergic Agonists: Mixed-Action Agents01:28

Adrenergic Agonists: Mixed-Action Agents

Mixed-action adrenergic agonists, like ephedrine and pseudoephedrine, directly and indirectly affect adrenergic receptors. These agents stimulate adrenoceptors and indirectly release stored neurotransmitters, amplifying the adrenergic response.
Ephedrine and pseudoephedrine lack a catecholamine group, making them less susceptible to degradation by metabolic enzymes. They have increased oral bioavailability and lipophilicity, resulting in a longer duration of action. Their response is reduced by...
Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers01:22

Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers

α-Adrenergic antagonists, known as α-blockers, exert their effects by inhibiting α-adrenoceptors, leading to specific physiological actions. α1-blockers and α2-blockers have distinct pharmacological actions and therapeutic applications.
α1-blockers: These drugs inhibit α1-adrenoceptors on smooth muscle cells, resulting in vasodilation. This vasodilation lowers blood pressure, making α1-blockers valuable in treating hypertension. Additionally, α1-blockers effectively address urinary obstruction...
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...
Stimulants01:29

Stimulants

Stimulants are substances that enhance neural activity and elevate dopamine levels in the brain, leading to their highly addictive nature. These drugs include cocaine, amphetamines, MDMA, caffeine, and nicotine, each with distinct mechanisms of action and varied health implications.
Cocaine can be administered via snorting, injection, or smoking. It primarily functions by blocking the reuptake of dopamine, resulting in a euphoric high characterized by an intense sensation of happiness and...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Superoxide-driven oxi-inflammatory activation in PBMC cultures: evidence supporting a cellular ageing trigger.

Free radical research·2026
Same author

Redox-driven mechanisms link pesticide-induced microglial immunotoxicity to neurobehavioural impairment in an invertebrate ecotoxicological model.

Environmental toxicology and pharmacology·2026
Same author

Cocoa Bean Shell as a Functional Food By-Product: Antioxidant Potential and Toxicological Thresholds in <i>Drosophila melanogaster</i>.

Food science & nutrition·2026
Same author

Skin Aging and Mitochondrial Dysfunction: Structural Changes, Mechanistic Insights, and Therapeutic Perspectives.

Oxidative medicine and cellular longevity·2026
Same author

Mitochondrial Impairment Associated With Dopaminergic Neurotoxicity Following Exposure to Manganese and Methylmercury in Caenorhabditis elegans.

Journal of biochemical and molecular toxicology·2025
Same author

Physicochemical and Toxicity Study of Naringin-Loaded Chitosan Nanocapsules.

Journal of biomedical materials research. Part B, Applied biomaterials·2025

Related Experiment Video

Updated: Jun 26, 2026

Rapid High-throughput Species Identification of Botanical Material Using Direct Analysis in Real Time High Resolution Mass Spectrometry
11:14

Rapid High-throughput Species Identification of Botanical Material Using Direct Analysis in Real Time High Resolution Mass Spectrometry

Published on: October 2, 2016

Guarana (

Daniele Coradini Zamberlan1, Leticia Priscilla Arantes1, Marina Lopes Machado1

  • 1Laboratório de Neuroproteção e Neurotoxicologia Experimental, Departamento de Bioquímica e Biologia Molecular, CCNE, Universidade Federal de Santa Maria, RS, Brazil.

Nutritional Neuroscience
|September 11, 2018
PubMed
Summary

Guarana extract (GEE) reduces amyloid-beta (Aβ) plaque formation and toxicity in a C. elegans Alzheimer

Keywords:
Alzheimer’sNeurodegenerative diseasesheat shock factor-1heat shock proteinsnatural compoundsproteostase

More Related Videos

Caffeine Extraction, Enzymatic Activity and Gene Expression of Caffeine Synthase from Plant Cell Suspensions
09:11

Caffeine Extraction, Enzymatic Activity and Gene Expression of Caffeine Synthase from Plant Cell Suspensions

Published on: October 2, 2018

Preparation of Hard Palm Seeds for Matrix-Assisted Laser Desorption/Ionization-Imaging Mass Spectrometry Analysis
07:55

Preparation of Hard Palm Seeds for Matrix-Assisted Laser Desorption/Ionization-Imaging Mass Spectrometry Analysis

Published on: June 30, 2023

Related Experiment Videos

Last Updated: Jun 26, 2026

Rapid High-throughput Species Identification of Botanical Material Using Direct Analysis in Real Time High Resolution Mass Spectrometry
11:14

Rapid High-throughput Species Identification of Botanical Material Using Direct Analysis in Real Time High Resolution Mass Spectrometry

Published on: October 2, 2016

Caffeine Extraction, Enzymatic Activity and Gene Expression of Caffeine Synthase from Plant Cell Suspensions
09:11

Caffeine Extraction, Enzymatic Activity and Gene Expression of Caffeine Synthase from Plant Cell Suspensions

Published on: October 2, 2018

Preparation of Hard Palm Seeds for Matrix-Assisted Laser Desorption/Ionization-Imaging Mass Spectrometry Analysis
07:55

Preparation of Hard Palm Seeds for Matrix-Assisted Laser Desorption/Ionization-Imaging Mass Spectrometry Analysis

Published on: June 30, 2023

Area of Science:

  • Neuroscience
  • Gerontology
  • Pharmacology

Background:

  • Alzheimer disease (AD) is a leading cause of dementia, characterized by amyloid plaques.
  • Current AD treatments are limited, necessitating novel therapeutic strategies.
  • Paullinia cupana (guarana) is an Amazonian plant with reported anti-aging properties.

Purpose of the Study:

  • To investigate the effects of guarana ethanolic extract (GEE) on amyloid-beta (Aβ) toxicity in a C. elegans model of AD.
  • To analyze GEE's impact on Aβ aggregation, behavioral deficits, and oxidative stress.
  • To explore the role of heat shock response in GEE's neuroprotective effects.

Main Methods:

  • Utilized a C. elegans model engineered to express human amyloid-beta (Aβ).
  • Administered chronic guarana ethanolic extract (GEE) treatment.
  • Assessed behavioral phenotypes, oxidative damage markers, and Aβ protein expression.
  • Investigated the involvement of heat shock protein (HSP) pathways.

Main Results:

  • Chronic GEE consumption significantly decreased Aβ aggregate formation in C. elegans.
  • GEE treatment ameliorated Aβ-induced behavioral deficits and oxidative damage.
  • The beneficial effects of GEE were associated with the activation of the heat shock protein (HSP) response.

Conclusions:

  • Guarana ethanolic extract (GEE) demonstrates neuroprotective effects against Aβ toxicity.
  • GEE offers a potential natural alternative for combating amyloidogenic neurodegenerative diseases.
  • Activation of the heat shock response pathway is a key mechanism underlying GEE's benefits.