Sensory Deprivation Triggers Synaptic and Intrinsic Plasticity in the Hippocampus

Hila Milshtein-Parush, Samuel Frere, Limor Regev, Coren Lahav, Amit Benbenishty, Shamgar Ben-Eliyahu, Inbal Goshen, Inna Slutsky*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


Hippocampus, a temporal lobe structure involved in learning and memory, receives information from all sensory modalities. Despite extensive research on the role of sensory experience in cortical map plasticity, little is known about whether and how sensory experience regulates functioning of the hippocampal circuits. Here, we show that 9 ± 2 days of whisker deprivation during early mouse development depresses activity of CA3 pyramidal neurons by several principal mechanisms: decrease in release probability, increase in the fraction of silent synapses, and reduction in intrinsic excitability. As a result of deprivation-induced presynaptic inhibition, CA3-CA1 synaptic facilitation was augmented at high frequencies, shifting filtering properties of synapses. The changes in the AMPA-mediated synaptic transmission were accompanied by an increase in NR2B-containing NMDA receptors and a reduction in the AMPA/NMDA ratio. The observed reconfiguration of the CA3-CA1 connections may represent a homeostatic adaptation to augmentation in synaptic activity during the initial deprivation phase. In adult mice, tactile disuse diminished intrinsic excitability without altering synaptic facilitation. We suggest that sensory experience regulates computations performed by the hippocampus by tuning its synaptic and intrinsic characteristics.

Original languageAmerican English
Pages (from-to)3457-3470
Number of pages14
JournalCerebral Cortex
Issue number6
StatePublished - 1 Jun 2017

Bibliographical note

Publisher Copyright:
© The Author 2017. Published by Oxford University Press.


  • hippocampus
  • intrinsic excitability
  • sensory deprivation
  • synaptic plasticity
  • whisker trimming


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