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- Rong Ma, Minyi Xiao, and Bengt Gustafsson.
- Department of Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. Electronic address: rong.ma@gu.se.
- Neuroscience. 2016 Nov 19; 337: 27-36.
AbstractThe apical dendrite of hippocampal CA1 pyramidal cells receives information from the entorhinal cortex via the dentate gyrus and CA3 (Schaffer-collateral (SC) input) proximally within the stratum radiatum (SR) and directly from the entorhinal cortex/thalamus distally within the stratum lacunosum-moleculare (SLM). During the early postnatal development, very low/low frequency (0.033-1Hz) activation of previously non-stimulated (naïve) SC synapses (SR-CA1 synapses) results in a stimulus-, but not frequency-, dependent depression which is explained by postsynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) silencing. This lability of AMPA signaling has been suggested to play a role in the activity-dependent organization of the SR synaptic input. Compared with the SR region the SLM region is matured earlier and may become organized in a different manner. Here, using field recordings of synaptic activity in hippocampal slices from 2nd postnatal week rats, we found that SLM-CA1 synapses are also readily depressed by activity in the very low/low frequency range (0.033-1Hz). The depression was, however, quite distinct from that of SR-CA1 synapses, being frequency dependent and reversing faster following stimulus interruption. Bath application of an AMPA receptor agonist produced only a small (-8%) post-application (10min) depression of SLM-CA1 synapses in contrast to that of SR-CA1 synapses (-33%). The SLM-CA1 synapses did also exhibit less long-term depression than the SR-CA1 synapses. We conclude that in the developing hippocampus the labile glutamate signaling onto CA1 pyramidal cell depends mechanistically on input pathway. The labile AMPA signaling at SLM-CA1 synapses is most likely explained by a presynaptic mechanism with limited amount of postsynaptic AMPA silencing.Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.
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