Abstract
Action-potential-induced LTD (AP-LTD) is a form of synaptic plasticity that reduces synaptic strength in CA1 hippocampal neurons firing antidromically during sharp-wave ripples. This firing occurs during slow-wave sleep and quiet moments of wakefulness, which are periods of offline replay of neural sequences learned during encoding sensory information. Here we report that rapid and persistent down-regulation of different mRNA transcripts of the BDNF gene accompanies AP-LTD, and that AP-LTD is abolished in mice with the BDNF gene knocked out in CA1 hippocampal neurons. These findings increase understanding of the mechanism of AP-LTD and the cellular mechanisms of memory consolidation.
Highlights
Action-potential-induced LTD (AP-LTD) is a form of synaptic plasticity that reduces synaptic strength in CA1 hippocampal neurons firing antidromically during sharp-wave ripples
5′-end forward primers were designed that are specific for brain-derived neurotrophic factor (BDNF) exons I, IIc, IV, IX, and a 3′-end primer was generated that is complementary to sequences in exon IX, that is common to all BDNF transcripts, and used as reverse primer for all transcripts (Fig. 1A)
The results show that down regulation of BDNF mRNA abundance accompanies AP-LTD, and that expression of BDNF in CA1 of hippocampus is required for this form of synaptic plasticity, which is induced by antidromic firing in the absence of excitatory synaptic input
Summary
Action-potential-induced LTD (AP-LTD) is a form of synaptic plasticity that reduces synaptic strength in CA1 hippocampal neurons firing antidromically during sharp-wave ripples. This firing occurs during slow-wave sleep and quiet moments of wakefulness, which are periods of offline replay of neural sequences learned during encoding sensory information. The results show that AP-LTD is accompanied by a rapid reduction in BDNF mRNA abundance, with different exons showing different levels of regulation and different temporal responses, and that AP-LTD is impaired in mice with deletion of BDNF restricted to the CA1 region Together these results indicate that this form of synaptic plasticity, which is associated with SPW-Rs, requires BDNF downregulation
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