Research articleBDNF mRNA abundance regulated by antidromic action potentials and AP-LTD in hippocampus

- BDNF gene expression in hippocampal CA1 neurons is necessary for LTD induced by antidromic stimulation (AP-LTD).
- BDNF mRNA transcripts are rapidly downregulated during AP-LTD.
- Different BDNF mRNA transcripts respond with distinct temporal profiles to antidromic stimulation.
- In contrast to antidromic stimulation, abundance in BDNF mRNA increases after LTD induced chemically by activation of L-VDCC.

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.