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Coexistence of muscarinic long-term depression with electrically induced long-term potentiation and depression at CA3-CA1 synapses.

Coexistence of muscarinic long-term depression with electrically induced long-term potentiation and depression at CA3-CA1 synapses. Research Abstract Details 

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  • Coexistence of muscarinic long-term depression with electrically induced long-term potentiation and depression at CA3-CA1 synapses. Abstract Text:

    eve mccutchenEve McCutchen,cary l scheidererCary L Scheiderer,lynn e dobrunzLynn E Dobrunz,lori l mcmahonLori L McMahon,

    Our laboratory recently characterized a form of long-term depression (LTD) at CA3-CA1 synapses mediated by M1 muscarinic receptors (mAChRs), termed muscarinic LTD (mLTD). mLTD is both activity and NMDAR dependent, characteristics shared by forms of synaptic plasticity thought to be relevant to learning and memory, including long-term potentiation (LTP) induced by high-frequency stimulation (HFS-LTP) and long-term depression induced by low-frequency stimulation (LFS-LTD). However, it remains unclear whether mLTD can occur sequentially with these electrically induced forms of hippocampal plasticity or whether mLTD might interact with them. The first goal of this study was to examine the interplay of mLTD and HFS-LTP. We report that mLTD expression does not alter subsequent induction of HFS-LTP and, further, at synapses expressing HFS-LTP, mLTD can mediate a novel form of depotentiation. The second goal was to determine whether mLTD would alter LFS-LTD induction and/or expression. Although we show that mLTD is occluded by saturation of LFS-LTD, suggesting mechanistic similarity between these two plasticities, saturation of mLTD does not occlude LFS-LTD. Surprisingly, however, the LFS-LTD that follows cholinergic receptor activation is NMDAR independent, indicating that application of muscarinic agonist induces a change in the induction mechanism required for LFS-LTD. These data demonstrate that mLTD can coexist with electrically induced forms of synaptic plasticity and support the hypothesis that mLTD is one of the mechanisms by which the cholinergic system modulates hippocampal function.

    Coexistence of muscarinic long-term depression with electrically induced long-term potentiation and depression at CA3-CA1 synapses. Publishing Authors By Initials

    e mccutchenE McCutchen,cl scheidererCL Scheiderer,le dobrunzLE Dobrunz,ll mcmahonLL McMahon,

    For similar nervous system: synapses research abstracts see: nervous system: synapses research

    PUBMED ID PMID:

    MEDLINE DATE:

    Coexistence of muscarinic long-term depression with electrically induced long-term potentiation and depression at CA3-CA1 synapses. Journal Published:

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

    Journal: Journal of neurophysiology

    VOLUME: 96

    Page Numbers: 3114-21

    Journal Abbreviation: J. Neurophysiol.

    ISSN: 0022-3077

    DAY: 27

    MONTH: 09

    YEAR: 2006

    Coexistence of muscarinic long-term depression with electrically induced long-term potentiation and depression at CA3-CA1 synapses. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 375404

    Coexistence of muscarinic long-term depression with electrically induced long-term potentiation and depression at CA3-CA1 synapses. Keywords Mesh Terms:

    KEYWORDS: Synapses

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Coexistence of muscarinic long-term depression with electrically induced long-term potentiation and depression at CA3-CA1 synapses. Information

    Substance Name: 2-Amino-5-phosphonovalerate

    Registry Number: 76726-92-6

    Grant and Affiliation Information for Coexistence of muscarinic long-term depression with electrically induced long-term potentiation and depression at CA3-CA1 synapses.

    AFFILIATION: The University of Alabama at Birmingham, 1918 University Blvd, MCLM 964, Birmingham, AL 35294-0005, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIA

    GRANT: P50 AG 16582

    ACRONYM: AG

    MEDLINETA: J Neurophysiol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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