Abstract：
:Depotentiation, the reversal of long-term potentiation (LTP), can be induced by activation of metabotropic glutamate receptors (mGluRs) or NMDA receptors (NMDARs). Although NMDAR-dependent depotentiation is due to a protein phosphatase-dependent erasure of LTP, the notion that mGluR-dependent depotentiation also involves LTP erasure is controversial. To address this issue we used electrophysiological and biochemical approaches to investigate mGluR-dependent depotentiation in hippocampal slices. Activating group I mGluRs with (R,S)-3,5-dihydroxyphenylglycine (DHPG) induced robust depotentiation in both the CA1 and CA3 regions of hippocampal slices. Western immunoblotting of samples prepared from DHPG-treated slices revealed, however, that activation of group I mGluRs causes a transient increase in phosphorylation of AMPA receptor GluR1 subunits at sites crucial for LTP and under some conditions causes persistent activation of alphaCamKII. The paradoxical ability of DHPG to induce depotentiation while at the same time activating signaling pathways involved in LTP suggests that LTP might not be erased by mGluR-dependent depotentiation. Consistent with this, DHPG-induced depotentiation did not restore the ability of high-frequency stimulation to induce LTP at synapses that had previously undergone saturating levels of LTP. In addition, blocking the expression of DHPG-induced LTD revealed hidden LTP at depotentiated synapses. Our results indicate that LTP and mGluR-dependent LTD can co-exist at excitatory synapses.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Delgado JY,O'dell TJdoi
10.1016/j.neuropharm.2005.01.008subject
Has Abstractpub_date
2005-06-01 00:00:00pages
936-48issue
7eissn
0028-3908issn
1873-7064pii
S0028-3908(05)00038-9journal_volume
48pub_type
杂志文章abstract：:Sustained administration of opioids leads to antinociceptive tolerance, while prolonged association of L-type Ca2+ channel blockers (e.g. nimodipine) with opioids results in increased antinociceptive response. Herein, we investigated the changes in mu-opioid receptor signalling underlying this shift from analgesic tol...
journal_title：Neuropharmacology
pub_type： 杂志文章
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更新日期：2008-05-01 00:00:00
abstract：:Metabotropic glutamate (mGlu) receptors are implicated in many neurological and psychiatric diseases and are the targets of therapeutic agents currently in clinical development. Their activation has diverse effects in the central nervous system (CNS) that includes an involvement in synaptic plasticity. We previously r...
journal_title：Neuropharmacology
pub_type： 杂志文章
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更新日期：2013-11-01 00:00:00
abstract：:Microglial cells killed neurons damaged following incubation with sub-lethal concentrations of peptides derived from either the human prion protein (HuPrP82-146) or amyloid-beta1-42 (a peptide found in Alzheimer's disease). HuPrP82-146 or amyloid-beta1-42 induced phenotypic changes in neurons that caused them to bind ...
journal_title：Neuropharmacology
pub_type： 杂志文章
doi：10.1016/j.neuropharm.2005.09.008
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journal_title：Neuropharmacology
pub_type： 杂志文章,评审
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pub_type： 杂志文章
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journal_title：Neuropharmacology
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更新日期：2018-03-15 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
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更新日期：1991-01-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章,评审
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更新日期：2015-09-01 00:00:00
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pub_type： 杂志文章
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更新日期：2002-02-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
doi：10.1016/j.neuropharm.2005.10.008
更新日期：2006-03-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
doi：10.1016/j.neuropharm.2018.12.020
更新日期：2019-04-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
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更新日期：2018-06-01 00:00:00
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journal_title：Neuropharmacology
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更新日期：2019-01-01 00:00:00
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pub_type： 杂志文章
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journal_title：Neuropharmacology
pub_type： 杂志文章
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pub_type： 杂志文章
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pub_type： 杂志文章
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更新日期：2000-08-23 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
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更新日期：1997-04-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章,评审
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更新日期：2012-02-01 00:00:00
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pub_type： 杂志文章
doi：10.1016/j.neuropharm.2013.07.013
更新日期：2013-12-01 00:00:00
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journal_title：Neuropharmacology
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doi：10.1016/s0028-3908(03)00032-7
更新日期：2003-03-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
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更新日期：1995-11-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
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更新日期：1996-04-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
doi：10.1016/j.neuropharm.2018.08.015
更新日期：2018-10-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
doi：10.1016/j.neuropharm.2004.10.011
更新日期：2005-03-01 00:00:00
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journal_title：Neuropharmacology
pub_type： 杂志文章
doi：10.1016/0028-3908(84)90077-7
更新日期：1984-12-01 00:00:00
