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 Experiment Videos

Neuromuscular function and organotin compounds.

G G Bierkamper, E Aizenman, W R Millington

    Neurotoxicology
    |January 1, 1984
    PubMed
    Summary

    Triethyltin (TET) causes significant neurological damage, including hindlimb paralysis and impaired neurotransmission at the neuromuscular junction. This study investigates TET

    Related Concept Videos

    You might also read

    Related Articles

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

    Sort by
    Same author

    Hypovolemic hemorrhage induces Fos expression in the rat hypothalamus: Evidence for involvement of the lateral hypothalamus in the decompensatory phase of hemorrhage.

    Neuroscience·2016
    Same author

    SNARE-dependent upregulation of potassium chloride co-transporter 2 activity after metabotropic zinc receptor activation in rat cortical neurons in vitro.

    Neuroscience·2012
    Same author

    Complex role of zinc in methamphetamine toxicity in vitro.

    Neuroscience·2010
    Same author

    Preimplantation genetic diagnosis for BRCA1/2--a novel clinical experience.

    Prenatal diagnosis·2009
    Same author

    Laser-assisted derivation of human embryonic stem cell lines from IVF embryos after preimplantation genetic diagnosis.

    Human reproduction (Oxford, England)·2007
    Same author

    A vital role for voltage-dependent potassium channels in dopamine transporter-mediated 6-hydroxydopamine neurotoxicity.

    Neuroscience·2006

    Area of Science:

    • Neurotoxicology
    • Environmental Health
    • Cellular Biology

    Background:

    • Trialkyltin compounds, such as triethyltin (TET), are known neurotoxicants.
    • TET exposure in mammals leads to neurological damage, characterized by cerebral edema and muscle weakness.

    Purpose of the Study:

    • To investigate the pathological manifestations of triethyltin (TET) toxicity in the mammalian nervous system.
    • To elucidate the effects of TET on neuromuscular transmission and muscle function.

    Main Methods:

    • Oral administration of TET bromide to rats.
    • Histopathological examination of nervous system tissues and muscles.
    • Electrophysiological recordings of nerve conduction and neuromuscular junction activity in vivo and in vitro.

    Main Results:

    • TET exposure caused progressive hindlimb weakness, paresis, and paraplegia in rats.
    • Histopathology revealed intramyelinic vacuolization in ventral roots and spinal cord horn, with minimal peripheral nerve damage.
    • Neurotransmission at the neuromuscular junction was functionally depressed, with decreased acetylcholine release and altered endplate potentials.

    Conclusions:

    • TET toxicity primarily affects the central and peripheral nervous system, leading to motor deficits.
    • Impaired neuromuscular junction function significantly contributes to the muscular weakness observed in TET intoxication.
    • Further research is warranted to understand the precise mechanisms of TET-induced neurotoxicity.

    Related Experiment Videos