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

G Protein-coupled Receptors01:15

G Protein-coupled Receptors

G Protein-Coupled Receptors or GPCRs are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to sensory stimuli such as light, odors, hormones, cytokines, or neurotransmitters.
GPCRs are also called heptahelical, 7TM, or serpentine receptors, and consist of seven (H1-H7) transmembrane alpha-helices that span the bilayer to form a cylindrical core. The transmembrane helices are connected by three extracellular loops and three...
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...
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
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...
Targets for Drug Action: Overview01:26

Targets for Drug Action: Overview

Drugs target macromolecules to modify ongoing cellular processes. Primary drug targets include receptors, ion channels, transporters, and enzymes.
Receptors are either membrane-spanning or intracellular proteins, which upon binding a ligand, get activated and transmit the signal downstream to elicit a response. Drugs bind receptors, either mimicking the action of endogenous ligands or blocking the receptor activity to bring about a modified response. Nearly 35% of approved drugs target the G...

You might also read

Related Articles

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

Sort by
Same author

An Integrated Approach Combining Chemical Profiling, Network Pharmacology, and In Vitro Validation to Uncover the Multitarget Mechanisms of Naokang II Decoction against Vascular Dementia.

Journal of natural products·2026
Same author

Lithium Chloride Rescues Dopaminergic Neurons in a Parkinson's Disease Rat Model Challenged with Rotenone.

CNS & neurological disorders drug targets·2025
Same author

Beneficial Effects of Tilapia Fish Skin on Excisional Skin Wound Healing in a Type I Diabetic Rat Model.

Journal of biomedical materials research. Part B, Applied biomaterials·2024
Same author

AI molecular property prediction for Parkinson's Disease reveals potential repurposing drug candidates based on the increase of the expression of PINK1.

Computer methods and programs in biomedicine·2023
Same author

Radical Scavenging Is Not Involved in Thymoquinone-Induced Cell Protection in Neural Oxidative Stress Models.

Antioxidants (Basel, Switzerland)·2023
Same author

Oxoglutarate dehydrogenase complex controls glutamate-mediated neuronal death.

Redox biology·2023

Related Experiment Video

Updated: Jun 6, 2026

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model
08:15

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model

Published on: June 6, 2025

Ginsenosides and their CNS targets.

Khaled Radad1, Rudolf Moldzio, Wolf-Dieter Rausch

  • 1Department of Pathology, Faculty of Veterinary Medicine, Assiut University, Assiut 71526, Egypt. khaledradad@hotmail.com

CNS Neuroscience & Therapeutics
|December 15, 2010
PubMed
Summary

Ginsenosides, compounds from ginseng, show promising effects on the central nervous system (CNS). Research indicates they can stimulate brain function and protect against CNS disorders and neurodegenerative diseases.

Related Experiment Videos

Last Updated: Jun 6, 2026

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model
08:15

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model

Published on: June 6, 2025

Area of Science:

  • Pharmacology
  • Neuroscience
  • Natural Products Chemistry

Background:

  • Ginsenosides are key bioactive compounds in ginseng, extensively studied for their medicinal properties.
  • Recent research highlights significant beneficial effects of ginsenosides on the central nervous system (CNS).

Purpose of the Study:

  • To review recently reported actions of ginsenosides on various CNS targets.
  • To explore the therapeutic potential of ginsenosides in CNS disorders and neurodegenerative diseases.

Main Methods:

  • Review of in vitro and in vivo studies on ginsenosides' effects.
  • Analysis of pharmacological mechanisms, including effects on cerebral metabolism and oxidative stress.

Main Results:

  • Ginsenosides modulate cerebral metabolism, oxidative stress, neurotransmitter balance, and membrane stability.
  • These compounds exhibit antiapoptotic effects relevant to neuroprotection.
  • Evidence suggests ginsenosides can offer general brain stimulation and protection against CNS diseases.

Conclusions:

  • Ginsenosides possess multifaceted actions on the central nervous system.
  • Their demonstrated neuroprotective and neurostimulatory effects support their therapeutic potential for neurological conditions.