Reelin: Neurodevelopmental architect and homeostatic regulator of excitatory synapses

Catherine R. Wasser, Joachim Herz

Research output: Contribution to journalReview articlepeer-review

70 Scopus citations


Over half a century ago, D. S. Falconer first reported a mouse with a reeling gate. Four decades later, the Reln gene was isolated and identified as the cause of the reeler phenotype. Initial studies found that loss of Reelin, a large, secreted glycoprotein encoded by the Reln gene, results in abnormal neuronal layering throughout several regions of the brain. In the years since, the known functions of Reelin signaling in the brain have expanded to include multiple postdevelopmental neuromodulatory roles, revealing an ever increasing body of evidence to suggest that Reelin signaling is a critical player in the modulation of synaptic function. In writing this review, we intend to highlight the most fundamental aspects of Reelin signaling and integrate how these various neuromodulatory effects shape and protect synapses.

Original languageEnglish (US)
Pages (from-to)1330-1338
Number of pages9
JournalJournal of Biological Chemistry
Issue number4
StatePublished - Jan 27 2017

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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