Literature DB >> 10321460

Potentiation and depression following stimulus interruption in young rat hippocampi.

Y P Niu1, M Y Xiao, M Karpefors, H Wigström.   

Abstract

We examined the effect of stimulus interruption on dual component field EPSPs in the hippocampal CA1 region. Resuming test stimulation at 0.1 Hz after 10-60 min silent periods led to an increase of the response followed by a decline, involving AMPA and NMDA components to a similar extent. Similar changes were seen when stimulation was initially applied to a naive pathway or the stimulus strength was increased during an experiment. The potentiation of the AMPA response was largely blocked by prior application of the NMDA antagonist AP5 while application of this drug immediately after the initial potentiation prevented the following decline. The results demonstrate that NMDA-dependent potentiation and depression, possibly equivalent to LTP and LTD, can both be induced by the same, very low, test stimulus frequency. Furthermore, the depression appeared to have a longer time window for its induction than the potentiation.

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Year:  1999        PMID: 10321460     DOI: 10.1097/00001756-199904060-00005

Source DB:  PubMed          Journal:  Neuroreport        ISSN: 0959-4965            Impact factor:   1.837


  3 in total

1.  Studies of the mechanism of development of "deprivation" potentiation of population responses of neurons in field CA1 of living hippocampal slices.

Authors:  V A Popov; V A Markevich
Journal:  Neurosci Behav Physiol       Date:  2002 Nov-Dec

2.  Transient and sustained types of long-term potentiation in the CA1 area of the rat hippocampus.

Authors:  Arturas Volianskis; Morten S Jensen
Journal:  J Physiol       Date:  2003-06-06       Impact factor: 5.182

3.  Slowly developing depression of N-methyl-D-aspartate receptor mediated responses in young rat hippocampi.

Authors:  Mikhail Dozmorov; Rui Li; Hui-Ping Xu; Barbro Jilderos; Holger Wigström
Journal:  BMC Neurosci       Date:  2004-08-03       Impact factor: 3.288

  3 in total

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