Loss of limbic system-associated membrane protein leads to reduced hippocampal mineralocorticoid receptor expression, impaired synaptic plasticity, and spatial memory deficit

Shenfeng Qiu, Danielle L. Champagne, Melinda Peters, Elizabeth H. Catania, Edwin J. Weeber, Pat Levitt, Aurea F. Pimenta

Research output: Contribution to journalArticle

36 Scopus citations


Background: The limbic system-associated membrane protein (LAMP) promotes development of neurons of limbic origin. We have previously shown that genetic deletion of LAMP results in heightened reactivity to novelty and reduced anxiety-like behaviors in mice. Here, we demonstrate a critical role of LAMP in hippocampal-dependent synaptic physiology and behavior. Methods: We tested spatial memory performance, hippocampal synaptic plasticity, and stress-related modalities in Lsamp-/- mice and their littermate control mice. Results: Lsamp-/- mice exhibit a pronounced deficit in spatial memory acquisition and poorly sustained CA1 long-term potentiation. We found reduced expression of mineralocorticoid receptor (MR) transcripts in the hippocampus and reduction in the corticosterone-induced, MR-mediated nongenomic modulatory effects on CA1 synaptic transmission. Importantly, the impaired long-term potentiation in Lsamp-/- mice can be rescued by stress-like levels of corticosterone in a MR-dependent manner. Conclusions: Our study reveals a novel functional relationship between a cell adhesion molecule enriched in developing limbic circuits, glucocorticoid receptors, and cognitive functioning.

Original languageEnglish (US)
Pages (from-to)197-204
Number of pages8
JournalBiological Psychiatry
Issue number2
StatePublished - Jul 15 2010



  • Limbic system-associated membrane protein
  • mineralocorticoid receptor
  • spatial memory
  • stress
  • synaptic plasticity

ASJC Scopus subject areas

  • Biological Psychiatry

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