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Long‐lasting synaptic loss after repeated induction of LTD: independence to the means of LTD induction
Author(s) -
Kamikubo Yuji,
Egashira Yoshihiro,
Tanaka Tsunehiro,
Shinoda Yo,
TominagaYoshino Keiko,
Ogura Akihiko
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.05032.x
Subject(s) - metabotropic glutamate receptor , synaptic plasticity , long term potentiation , long term depression , neuroscience , synapse , neurotransmission , nmda receptor , glutamate receptor , synaptic augmentation , synaptic fatigue , metaplasticity , metabotropic receptor , ltp induction , biology , chemistry , excitatory postsynaptic potential , receptor , ampa receptor , inhibitory postsynaptic potential , biochemistry
Short‐ and long‐lasting synaptic plasticity is assumed to be the cellular basis of short‐ and long‐lasting memory, respectively. However, the cellular consequences leading to the long‐lasting synaptic plasticity, assumed to include the processes of synapse formation and elimination, remain unknown. Using hippocampal slices maintained stably in culture, we found previously that the repeated induction of long‐term potentiation (LTP) triggered a slowly developing long‐lasting enhancement in synaptic transmission strength accompanied by synapse formation, which was separate from LTP itself. We recently reported a phenomenon apparently of a mirror‐image effect. The repeated activations of metabotropic glutamate receptor (mGluR), which induces long‐term depression (LTD), triggered a long‐lasting reduction in synaptic strength accompanied by synapse elimination. To clarify whether the reported long‐lasting effect was specific to the drugs used previously and whether the effect was specific to mGluR‐mediated LTD, we exposed the cultured slices repeatedly to another Group I metabotropic glutamate receptor (mGluR) agonist, an N ‐methyl‐ d ‐aspartate receptor agonist, and a Na + /K + ‐pump inhibitor. All these treatments resulted in an equivalent long‐lasting synaptic reduction/elimination when repeated three times, indicating that the repeated LTD induction leads to synapse elimination. The independence of synapse elimination to the means of LTD induction suggests that the signals leading to short‐term plasticity and long‐term plasticity are independent. Detailed inspections in the representative case of mGluR activation revealed that the reduction in synaptic strength developed with a ∼1‐week delay from the decrease in the number of synaptic structures. This synapse elimination should be unique as it is activity‐dependent rather than inactivity‐dependent.