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

Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific...
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...
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

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...
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...
Local Anesthetics: Adverse Effects01:12

Local Anesthetics: Adverse Effects

While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
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...

You might also read

Related Articles

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

Sort by
Same author

Chronic prosthetic joint infection caused by Coxiella burnetii diagnosed by metagenomic next-generation sequencing: A case report and literature review.

Journal of infection and public health·2026
Same author

Artemisitene formation during UVA-assisted Fenton oxidation of arteannuin B.

Photochemistry and photobiology·2026
Same author

Study on the internal leakage pneumatic noise acoustic characteristics of spring-loaded full-lift safety valve.

Scientific reports·2026
Same author

Application of a deep learning method based on CBCT panoramic reconstruction images for differentiating operationally defined cystic and neoplastic jaw lesions from osteomyelitis: a single-center retrospective study.

Scientific reports·2026
Same author

NOD-like immune receptor Prf prevents ubiquitin-proteasome-mediated degradation of the defense-related transcription factor SlNAC1.

Plant physiology·2026
Same author

POTEF upregulation drives hepatocellular carcinoma progression via oncogenic signaling and immune modulation.

Scientific reports·2026

Related Experiment Video

Updated: May 8, 2026

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity
15:04

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity

Published on: May 5, 2009

25.4K

Comparative neurotoxic effects and mechanism of cadmium chloride and cadmium sulfate in neuronal cells.

Zongqin Mei1, Jie Yang2, Yuan Zhao1

  • 1Institute of Preventive Medicine, School of Public Health, Dali University, No. 22, Wanhua Road, Dali, Yunnan 671000, PR China; Institute of Preventive Medicine, Dali University, Dali, Yunnan, PR China.

Environment International
|August 31, 2025
PubMed
Summary

This study compares the neurotoxic effects of cadmium chloride (CdCl2) and cadmium sulfate (CdSO4) in cells and mice. Findings reveal cadmium-induced oxidative stress and DNA damage, impacting neurological function.

Keywords:
Cadmium chlorideCadmium sulphateNeurotoxicityProteomicsToxicity comparison

More Related Videos

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line
08:23

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

Published on: August 9, 2014

11.5K
Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons
15:05

Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons

Published on: February 5, 2015

9.5K

Related Experiment Videos

Last Updated: May 8, 2026

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity
15:04

A Neuronal and Astrocyte Co-Culture Assay for High Content Analysis of Neurotoxicity

Published on: May 5, 2009

25.4K
Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line
08:23

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

Published on: August 9, 2014

11.5K
Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons
15:05

Functional Evaluation of Biological Neurotoxins in Networked Cultures of Stem Cell-derived Central Nervous System Neurons

Published on: February 5, 2015

9.5K

Area of Science:

  • Neuroscience
  • Toxicology
  • Molecular Biology

Background:

  • Cadmium (Cd) is a food pollutant known to cause neurological damage.
  • Cadmium chloride (CdCl2) and cadmium sulfate (CdSO4) are implicated in oxidative stress and apoptosis.
  • Differential concentration-dependent neurotoxic effects and mechanisms of CdCl2 and CdSO4 require further elucidation.

Purpose of the Study:

  • To investigate the differential neurotoxic effects of CdCl2 and CdSO4.
  • To elucidate the underlying mechanisms of cadmium-induced neurotoxicity.
  • To compare the concentration-dependent toxicity of CdCl2 and CdSO4 in neuronal cells and a mouse model.

Main Methods:

  • PC12 cells treated with varying concentrations of CdCl2 and CdSO4.
  • C57BL/6J mice exposed to CdSO4 in drinking water.
  • Non-labeled quantitative proteomics and bioinformatics analysis.

Main Results:

  • Both CdCl2 and CdSO4 induced oxidative damage, genetic material damage, and apoptosis in PC12 cells.
  • CdCl2 showed higher toxicity than CdSO4 at lower concentrations, and lower toxicity at higher concentrations.
  • Proteomics revealed involvement of oxidative stress, DNA damage/repair pathways (e.g., Base excision repair, DNA replication), and identified differential expression of key proteins (Nrf2, Hmox1, Gsta3, Nqo1, Pole).

Conclusions:

  • Cadmium exposure leads to oxidative damage and impaired DNA repair in neuronal cells, ultimately inducing cell death.
  • The study provides the first comprehensive comparison of CdCl2 and CdSO4 neurotoxicity.
  • Cadmium-induced neurotoxicity may be mediated through the Nrf2/Hmox1/Gsta3/Nqo1/Pole signaling pathway.