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TENS stimulates constitutive nitric oxide release via opiate signaling in invertebrate neural tissues.

TENS stimulates constitutive nitric oxide release via opiate signaling in invertebrate neural tissues. Research Abstract Details 

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  • TENS stimulates constitutive nitric oxide release via opiate signaling in invertebrate neural tissues. Abstract Text:

    jeanette chengJeanette Cheng,chen zhangChen Zhang,ji-sheng hanJi-Sheng Han,george b stefanoGeorge B Stefano,richard m kreamRichard M Kream,

    BACKGROUND: There is a major societal concern relating to the addictive properties of analgesic drugs such as morphine with regard to alleviating pain. Because of this, alternative methods of pain relief are, and have been, actively pursued. An extremely promising method for treatment of low to moderate levels of chronic pain in humans is transcutaneous electrical nerve stimulation (TENS). MATERIAL/METHODS: All experiments utilized the invertebrate marine bivalve mollusc Mytilus edulis pedal ganglia. TENS was achieved using a stimulation apparatus developed by Professor Han of Peking University. TENS experiments employed 2 stimulation protocols: 1) low 2 Hz frequency at 5 mA current, 2) alternating low and high frequencies at 2 and 100 Hz, respectively at 5 mA current. Real-time measurements of nitric oxide (NO), using an amperometric probe, measured NO released into the tissue bath subsequent to TENS. RESULTS: Pooled M. edulis pedal ganglia exposed to TENS demonstrate that stimulation at 2 Hz and 5 mA current promotes time-dependent release of NO. In another experiment, pooled ganglia were stimulated at alternating frequencies of 2 Hz and 100 Hz and 5 mA, which also released NO in a time-dependent manner. Unstimulated control ganglia did not release significant amounts of NO. NO release was antagonized by naloxone and L-NAME exposure, demonstrating that it was receptor and nitric oxide synthase mediated, respectively. CONCLUSIONS: It would appear that TENS stimulates endogenous morphine release since NO release was blocked by naloxone and opioid peptides do not release NO. The present study is highly suggestive of the occurrence of this same mechanism in mammalian neural systems since all biochemical and signaling components are present. Furthermore, it would appear that this process has evolutionary survival value since it occurs in an animal that evolved 500 million years ago.

    TENS stimulates constitutive nitric oxide release via opiate signaling in invertebrate neural tissues. Publishing Authors By Initials

    j chengJ Cheng,c zhangC Zhang,js hanJS Han,gb stefanoGB Stefano,rm kreamRM Kream,

    For similar abstracts research abstracts see: abstracts research

    PUBMED ID PMID:

    MEDLINE DATE:

    TENS stimulates constitutive nitric oxide release via opiate signaling in invertebrate neural tissues. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Medical science monitor : international medical jo

    VOLUME: 13

    Page Numbers: BR163-7

    Journal Abbreviation: Med. Sci. Monit.

    ISSN: 1234-1010

    DAY: 3

    MONTH: Aug

    YEAR: 2007

    TENS stimulates constitutive nitric oxide release via opiate signaling in invertebrate neural tissues. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9609063

    TENS stimulates constitutive nitric oxide release via opiate signaling in invertebrate neural tissues. Keywords Mesh Terms:

    KEYWORDS: Transcutaneous Electric Nerve Stimulatio

    MESH TERMS: methods

    Chemical & Substance for Abstract: TENS stimulates constitutive nitric oxide release via opiate signaling in invertebrate neural tissues. Information

    Substance Name: Morphine

    Registry Number: 57-27-2

    Grant and Affiliation Information for TENS stimulates constitutive nitric oxide release via opiate signaling in invertebrate neural tissues.

    AFFILIATION: Neuroscience Research Institute, State University of New York - College at Old Westbury, Old Westbury, NY 11568, USA.

    Country: Poland

    Poland Research PublicationPoland Research Publication

    AGENCY: United States NIMH

    GRANT: MH 47392

    ACRONYM: MH

    MEDLINETA: Med Sci Monit

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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