Astrocyte-mediated switch in spike timing-dependent plasticity during hippocampal development
Presynaptic spike timing-dependent long-term depression (t-LTD) at hippocampal CA3-CA1 synapses is evident until the 3 rd postnatal week in mice, disappearing during the 4 th week. At more mature stages, we found that the protocol that induced t-LTD induced t-LTP. We characterized this form of t-LTP...
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Veröffentlicht in: | Nature communications 2020-09, Vol.11 (1), p.4388-4388, Article 4388 |
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Sprache: | eng |
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Zusammenfassung: | Presynaptic spike timing-dependent long-term depression (t-LTD) at hippocampal CA3-CA1 synapses is evident until the 3
rd
postnatal week in mice, disappearing during the 4
th
week. At more mature stages, we found that the protocol that induced t-LTD induced t-LTP. We characterized this form of t-LTP and the mechanisms involved in its induction, as well as that driving this switch from t-LTD to t-LTP. We found that this t-LTP is expressed presynaptically at CA3-CA1 synapses, as witnessed by coefficient of variation, number of failures, paired-pulse ratio and miniature responses analysis. Additionally, this form of presynaptic t-LTP does not require NMDARs but the activation of mGluRs and the entry of Ca
2+
into the postsynaptic neuron through L-type voltage-dependent Ca
2+
channels and the release of Ca
2+
from intracellular stores. Nitric oxide is also required as a messenger from the postsynaptic neuron. Crucially, the release of adenosine and glutamate by astrocytes is required for t-LTP induction and for the switch from t-LTD to t-LTP. Thus, we have discovered a developmental switch of synaptic transmission from t-LTD to t-LTP at hippocampal CA3-CA1 synapses in which astrocytes play a central role and revealed a form of presynaptic LTP and the rules for its induction.
Presynaptic spike timing-dependent long-term depression at hippocampal CA3-CA1 synapses is evident until the third postnatal week in mice. The authors show that maturation beyond four weeks is associated with a switch to long-term potentiation in which astrocytes play a central role. |
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ISSN: | 2041-1723 2041-1723 |
DOI: | 10.1038/s41467-020-18024-4 |