Endoplasmic reticulum visiting spines is much more than a pretty movie, keeps synaptic strength from going through the roof! Out now👉https://t.co/FpSD6zumdx in @NatureComms! Ultimate privilege to study synapses with @OertnerLab. Grateful to @EMBO and #DFG
What is the endoplasmic reticulum (ER) doing in dendritic spines? It prevents runaway potentiation of excitatory synapses! Read about it in my last paper @OertnerLab.
Here 👇https://t.co/ZCOrB5GCMf Below: ER=green; cytosol=magenta (1/10)
(Almost) all you need to know about the effects of anesthesia on the hippocampus. CA1 population dynamics, spine turnover, memory consolidation. Now updated with comparison to sleep, CA1 activity during 6h post anesthesia, layer-specific effects, and more: https://t.co/0eQglHhi3O
Endoplasmic reticulum visiting spines is much more than a pretty movie, keeps synaptic strength from going through the roof! Out now👉https://t.co/FpSD6zumdx in @NatureComms! Ultimate privilege to study synapses with @OertnerLab. Grateful to @EMBO and #DFG
What is the endoplasmic reticulum (ER) doing in dendritic spines? It prevents runaway potentiation of excitatory synapses! Read about it in my last paper @OertnerLab.
Here 👇https://t.co/ZCOrB5GCMf Below: ER=green; cytosol=magenta (1/10)
Very excited to share our preprint on how time and space affect cFos ensembles in the dentate gyrus (DG), where we (@OertnerLab) combined #optogenetics and cFos-dependent tagging in the Morris water maze https://t.co/lV3zdnlB1F
@OKaneCahir This organelle pervades almost the entire neuron. EM studies showed that most spines in pyramidal neurons are devoid of ER. Our time-lapse analysis shows that this is just a matter of time and activity. ER will enter synapses as they go through periods of intense activity.
@YuriEliasR Excellent question. We don't know yet. Transient ER could be providing some sort of calcium signal triggered via CICR or mGluR-IP3, but also act as buffer. Last two scenarios are compatible with the lack of ER visits bringing about a potentiated state.
What is the endoplasmic reticulum (ER) doing in dendritic spines? It prevents runaway potentiation of excitatory synapses! Read about it in my last paper @OertnerLab.
Here 👇https://t.co/ZCOrB5GCMf Below: ER=green; cytosol=magenta (1/10)
We think that ER visits provide a brake mechanism at excitatory synapses during potentiation, thus keeping synaptic strength in check and allowing bidirectional synaptic plasticity. (10/10)
We wondered whether basal synaptic strength was altered in those neurons with impaired ER dynamics. Distribution of SEP-GluA2 showed enhanced spine enrichment of AMPA receptors. Two-photon glutamate uncaging on individual spines revealed higher AMPA and NMDA currents. (9/10)